1. Introduction
1.1. Yeasts
Yeasts, a group of around 1500 single-celled fungi species, are found in sugary media like fruit nectar and flower nectar, and have been traditionally used in the production of bread, beer, and wine [1]. They are eukaryotic organisms with a diameter of around 0.075 mm and can be spherical, egg-shaped, or filamentous [1]. Most yeasts reproduce asexually through budding, while some split into two equal cells through fission [1].
Yeasts are used in food production, where they produce carbon dioxide and ethanol through fermentation. These byproducts are used in bakery products, beer, and wine making. Yeast cells can ferment about their own weight of glucose in an hour [1]. Yeast for baking is available in two forms: compacted cakes with starch or dry grains mixed with cornmeal [1]. Commercial yeast is rich in niacin, folic acid, vitamins B1, B2, and B2, and has a 50% protein content. Deactivated brewer’s yeast and nutritional yeast can be taken as vitamin supplements [1].
Figure 1. Diversity of outlets involving yeast biotechnology roles [3].
Yeast identification involves physiological and morphological assays, including auxanography for determining carbon and nitrogen sources. Auxanography is a study that determines the growth of mutants which require specific substances to develop [2]. Systems like BCCM/Allev 2.00 and API strips analyze sugar absorption and fermentation. Yeasts inhabit diverse environments such as plant tissues, air, water, and land, with some thriving in solute-rich, extreme conditions. Species like S. cerevisiae colonize wine, while others are found in hospitals or cause food spoilage [3] (Figure 1).
Saccharomyces cerevisiae relies on fermentation for energy, even in the presence of oxygen. When glucose is scarce, it switches to using ethanol as a carbon source, triggering a shift in gene expression to favor gluconeogenesis (metabolic reactions that maintain blood glucose levels constant after digestion) [4] and the glyoxylate cycle (a variant of the tricarboxylic cycle found in plants, fungi and protists, permitting the use of two carbon compounds, when glucose is not present) [5], while reducing fermentation-related genes. Zinc cluster proteins like Cat8, Sip4, Rds2, and Adr1 drive this gene reprogramming.
NAD+ + 2e− + H+ ◊ Reduced NAD (NADH + H+) (Figure 2)
Figure 2. Cellular respiration and fermentation overview [6].
1.2. Sunscreens
The standard erythema dose (SED) measures the biological efficiency of UV radiation, specifically its ability to cause erythema (skin reddening). Sunscreens, although often applied less thoroughly than in SPF testing, can reduce sunburn cells, DNA damage, and risks of skin cancer such as actinic keratoses and squamous cell carcinomas. Chronic UV exposure is the leading cause of malignant melanoma and contributes to both photoaging and photo carcinogenesis [7]. Inorganic sunscreens like zinc oxide and titanium dioxide are effective and increasingly popular due to improved formulations [7]. SPF remains a key measure of sunscreen efficacy, and recent advancements have combined UV filters with DNA repair agents to enhance skin protection [7].
Extraterrestrial sunlight at sea level includes electromagnetic radiation from 290 to 3000 nm, with UV radiation categorized into UVA (320 - 400 nm), UVB (290 - 320 nm), and UVC (200 - 290 nm). While UVA predominates at the Earth’s surface, UVC is fully absorbed by the ozone layer. Variations in UV radiation depend on latitude, time of day, and season. The depletion of the ozone layer due to pollutants like nitric oxides and chlorofluorocarbons could increase UVB and UVC exposure, raising risks of skin cancer, photo immunosuppression, premature aging, and photosensitive diseases [8].
UV radiation, prevalent in the environment, contributes to skin diseases like inflammation, aging, and cancer. Personal exposure depends on sunlight intensity, time outdoors, and protective measures like clothing and sunscreen [9].
UVB and UVA radiation damage skin biomolecules, with UVB directly causing DNA lesions that can lead to mutations and skin cancer, particularly involving p53 mutations. The majority of p53 mutations are missense mutations, which produce full-length mutant p53 proteins. In addition to losing their ability to inhibit malignancies in a way dependent on wild-type p53, mutant p53 (Mutp53) proteins frequently acquire oncogenic gain-of-functions (GOF) that promote tumor growth [10]. UVA contributes to photoaging and suppresses the immune system. Photoprotection, including sun avoidance, protective clothing, and sunscreen, is central for preventing skin damage, photo immunosuppression, and skin cancers, and has become a major public health approach [10] [11].
Octinoxate, a common UVB absorber, is well-tolerated but degrades under sunlight, reducing its effectiveness. Encapsulation in nanoparticles can enhance their photostability. Avobenzone (Parsol 1789) is a strong UVA filter, but stabilizers may be needed to prevent degradation. Benzophenone-3, widely used and highly bioavailable, has a higher incidence of photodermatitis. Diethylamino hydroxybenzyl hexyl benzoate, more photostable than avobenzone, offers similar protection [12].
Photostability and Water Resistance
Photostability is essential for sunscreen effectiveness, ensuring it maintains its protective properties under sunlight. Some chemical filters, like octyl dimethyl PABA and avobenzone, can be photoreactive, reducing stability. Other filters, such as zinc oxide (ZnO), titanium dioxide (TiO2), salicylates, and methyl benzylidene camphor, enhance photostability, helping sunscreens better absorb, reflect, and scatter UV rays while remaining stable [13].
Sunscreen effectiveness in water is assessed by its ability to maintain SPF after immersion. In Europe, sunscreens are classified as “water-resistant” or “extra water-resistant” if post-immersion SPF remains at least 50% of the initial value after 40 or 80 minutes in water. The SPF label in the US reflects the pre-water exposure value [14].
Sunscreens and Melanoma
The link between sunscreen use and melanoma risk is debated, with studies showing conflicting results. Some suggest lower melanoma incidence with sunscreen use [15], while others indicate no significant impact [16]. A meta-analysis found little correlation, likely due to varying study methods and early sunscreens providing only UVB protection [17]. Modern sunscreens with broad-spectrum protection are still essential for preventing sunburn and mutations linked to melanoma, though their effectiveness against melanoma needs further study. Recent trials hint that sunscreens might reduce the risk of developing melanocytic naevi, a melanoma precursor [15] [16].
Cutaneous Responses to UV
UV radiation impacts skin physiology both immediately and over time [18]. Acute effects include inflammation, or “sunburn,” triggered by cytokines, which are small proteins that control the development and operation of blood cells and other immune system components [19], and other mediators, leading to keratinocyte apoptosis [19]. UV exposure also causes hyperkeratosis (thickening of the epidermis) and activates damage responses, such as p53-mediated cell cycle arrest and DNA repair [18]. The organism used in this investigation, yeast, has a similar mechanism. Tanning, an adaptive response, increases melanin production to protect against further UV damage, though defects in this process can raise cancer risk. UV light also affects immune function and converts 7-dehydrocholesterol into vitamin D3 [9]. UVA mainly causes oxidative damage, while UVB directly damages DNA, with ongoing research into their effects on the skin [9].
Oxidative Injury
Figure 3. UV photons generate oxidative free radicals, causing structural and functional changes in macromolecules like DNA, RNA, protein, and lipids. Enzymes like glutathione peroxidase, catalase, and superoxide dismutase detoxify these species. Adapted from: https://www.researchgate.net/figure/UV-generates-oxidative-free-radicals-UV-photons-interact-with-atomic-oxygen-to-promote_fig5_237095045
UV light generates reactive oxygen species (ROS), leading to mutations [20]. ROS causes nucleotide damage, resulting in mispairing and mutagenesis, such as the guanine-to-thymine mutation via 8-hydroxy-2’-deoxyguanine (8-OHdG), linked to skin cancer [21]. The base excision repair (BER) pathway repairs DNA damage, with glycosylases identifying and removing altered bases [20]. Antioxidant systems, including glutathione, superoxide dismutase (SODs), and catalase, detoxify ROS, protecting DNA and other macromolecules from UV-induced damage. These processes are crucial in managing the skin’s response to UV radiation [20] (Figure 3).
2. Research Question
How does exposure time to ambient ultraviolet (UV) radiation (0, 15, 30, 60 minutes) affect the rate of respiration, indicating the death toll of the yeast cells, and survival of yeast (Saccharomyces cerevisiae) by measuring carbon dioxide production (in ppm, ±10) and cell viability through the density in spectrophotometer, in the presence and absence of sunscreen?
3. Hypothesis
It is expected that without the presence of sunscreen, as exposure to ultraviolet radiation increases the rate of respiration of yeast and the number of yeast cells surviving will decrease. This is because exposure to UV radiation, damages the yeast cells. This is expected to be more evident at the high exposure time (60 minutes). On the other hand, in the presence of sunscreen it is expected that most yeast cells will survive, and the rate of respiration will also increase. Hence, there will be an increase in the amount of carbon dioxide produced.
4. Variables
4.1. Independent Variables
1) Presence of 9 ml/50ml yeast solution, or absence of Frezyderm Seaside sunscreen UV protection level 50+. The reason that that 9 ml of sunscreen were used per 50 ml of the yeast solution is that it was the minimum amount of sunscreen that created a thin layer on the surface of the solution. The aim was for this surface to be as thin as possible for it to not be embedded in the yeast solution and affect it even more. Also, after having tested different amounts of sunscreen and mixing the sunscreen with the yeast solution, the best outcome was with 9 ml, where only a thin layer was formed. In the other cases, there needed more titrations, leading to a greater error.
2) Time in minutes (0.0 min, 15.0 min, 30.0 min, 60.0 min, ±0.1 min) of exposure to ultra-violet radiation. The solution was placed in natural UV light, so that it could be exposed in the variety of wavelengths and natural conditions, and not only in the UV chamber which has only UVC. Also, these specific time periods were chosen for various of reasons. Firstly, 0.0 was chosen, to have a control variable which would not be exposed to the UV light at all, so that it could be comparable with the rest of the results. Also, this way, there is a better understanding of if the increase or decrease in CO2, or in the number of cells, was caused by contact inhibition of the yeast, mutations, or actually due to the UV radiation. More specifically, in contact inhibition, there is the factor of the toxic products that are attained and finally create a toxic environment which causes the death of the cells. Overpopulation is the main cause of this, when mutations may also be fatal.
In Table A1 (Appendix A), the ingredients of the sunscreen Frezyderm Seaside sunscreen UV protection level 50+ [22] are presented. To further understand its role, the purposes and the specific wavelength of UV radiation they present are listed.
4.2. Dependent Variables
1) Rate of respiration of yeast (Saccharomyces cerevisiae) by measuring the volume of carbon dioxide gas produced (ppm) using a carbon dioxide sensor (±10 ppm). CO2 will be measured so as to understand if the UV radiation causes cells to die or increases their rate of division. If cells die, then CO2 will decrease, since the rate of respiration will decrease, and even stop for some cells (the ones that will die). If UV radiation causes mutations, then CO2 will increase, since more cells will be respiring.
2) Number of yeast cells surviving measured using a spectrophotometer (absorbance). This number will be measured to understand if the UV radiation causes cells to die or mutate and increase in number. To convert absorbance to density, N = 0.125 * r was used, where N is the density, and r is the number of times which the sample is diluted [23]. If UV radiation kills the cells, then the density after exposure will decreases. On the other hand, if it causes mutations, then the cell density will increase.
In Table 1, the controlled variables are stated. Specifically, the reason and the way they were held constant is presented.
4.3. Controlled Variables
Table 1. Controlled variables, reasons for control, and the method of control.
Controlled variable |
Reason for control |
Method of control |
Volume of yeast solution used per trial |
So that the same number of yeast organisms are present in each trial |
50 ml measured using a volumetric cylinder |
Type of yeast (Saccharomyces cerevisae) used per trial |
Different yeasts may carry out respiration at different rates and may be affected by UV radiation in different ways |
Dry baker’s yeast |
Volume of Frezyderm seaside sunscreen used per trial |
So that the same number of sunscreen molecules are present for each different time of exposure |
9.0 ml measured using a volumetric cylinder |
Number of trials per exposure to UV radiation |
So that the experiment is fair and so that sufficient data can be collected |
5 trials per condition |
Temperature of water bath used for the control trials |
As all samples which were exposed to UV radiation where at an ambient temperature of 36˚C, the control yeasts were placed in an electronic water bath at the same temperature |
Water bath set at 36˚C and monitored using a thermometer |
Duration that the yeast was allowed to respire for before
and after UV exposure |
So that the experiment is fair and so that each yeast is given the same time to respire |
10 minutes each measured using a digital timer |
Speed of stirring yeast solution |
So that the mixing of yeast and water was at the same intensity |
Magnetic stirrer set at speed number 9 |
Speed of stirring while yeast solution was allowed to
respire |
So that the mixing of yeast and water was at the same intensity |
Magnetic stirrer set at speed number 2 |
Location of experimental setup while exposing yeast to UV radiation |
To allow for the same ambient temperature and amount of UV
radiation |
All trials were carried out outdoors, while also checking daily for the weather, UV index, and ambient temperature (information can be found in Figures A1-A3 in Appendix A) |
5. Materials and Apparatus
Dry baker’s yeast (Saccharomyces cerevisiae), 7.5 grams
Tap water, 2000 ml
Frezyderm Seaside sunscreen UV protection level 50+, 54 ml
Electronic weighing scale (±0.0002 g)
Magnetic stirrer
Carbon dioxide sensor
PASCO Capstone program
Conical flask 200 ml (±25 ml)
Volumetric cylinder 50 ml (±2.5 ml)
Volumetric cylinder 250 ml (±10 ml)
Beaker 50 ml (±5 ml)
Beaker 500 ml (±50 ml)
Spatula
Hot plate
Electronic water bath set at 36˚C
Thermometer
Digital timer (±0.1 s)
Plastic pipette
Glass stirring rod
Permanent marker
Tweezer
6. Method
6.1. Part A: Measuring Carbon Dioxide
1) 500 ml of tap water was measured using a volumetric cylinder and added to a beaker.
2) 2.5 grams of dry yeast were measured using an electronic weighing scale and added to the beaker containing the water.
3) The beaker was placed on a hot plate and a magnetic stirrer was added.
4) The stirrer was switched on at speed 9 and was allowed to stir until all the yeast had dissolved.
5) 50 ml of yeast solution was measured using a volumetric cylinder and added to a 250 ml conical flask
6) 9 ml of sunscreen was measured using a volumetric cylinder and added into the conical flask containing the 50 ml yeast forming a protective layer.
7) A small magnetic stirrer was added and switched on at speed 2.
8) The carbon dioxide sensor was placed in position at the opening of the conical flask.
9) RUN was pressed on the PASCO Capstone program and the levels of carbon dioxide (in ppm) were measured for 10 minutes.
10) The flask was then taken outdoors and sat under UV radiation for 60 minutes.
11) Steps 8 and 9 were repeated.
12) Steps 5 - 10 were repeated four more times.
13) Steps 5 - 12 were repeated for the remaining exposure times (15 min, 30 min)
14) Steps 1 - 13 were repeated in the absence of sunscreen (without step 6).
15) For the control (0 min exposure) steps 1 - 6 were repeated.
16) The conical flask was placed in an electronic water bath set at 36˚C until the mixture reached the desired temperature.
17) Steps 7 - 9 were repeated.
18) Steps 15 - 17 were repeated in the absence of sunscreen.
6.2. Part B: Measuring Number of Yeast Cells
1) 500 ml of tap water was measured using a volumetric cylinder and added to a beaker.
2) 2.5 grams of dry yeast were measured using an electronic weighing scale and added to the beaker containing the water.
3) The beaker was placed on a hot plate and a magnetic stirrer was added.
4) The stirrer was switched on at speed 9 and was allowed to stir until all the yeast had dissolved.
5) 3 ml of distilled water were measured using a plastic pipette and poured in 1 glass cuvette as the control measurement.
6) 3 ml of the yeast solution were measured using a plastic pipette and poured in 1 glass cuvette.
7) The two glass cuvettes were placed in the 2nd and 3rd slots of the spectrophotometer respectively.
8) Calibration at the distilled water took place, until it reached exactly 100%.
9) The drawer with the two cuvettes was moved and the cuvette with the solution was now in front of the light source.
10) The % mode was changed to the absorption setting.
11) Time passed until the absorbance was stable.
12) Dilutions were done until the absorbance was equal to 0.125.
13) Calculations were made to convert the absorbance into density (N = 0.125 * r).
14) 50 ml of yeast solution was measured using a volumetric cylinder and added to a 250 ml conical flask.
15) 9 ml of sunscreen was measured using a volumetric cylinder and added into the conical flask containing the 50 ml yeast forming a protective layer.
16) 4 conical flasks were prepared without sunscreen and 4 with sunscreen, with each the 50 ml of yeast solution.
17) One of each category of the conical flaks were the control measurements which were not exposed to the sun at all.
18) 1 of each flask was then exposed to the sun for 15 min, 30 min, 60 min.
19) After each period steps 5 - 13 were repeated.
7. Data Collection
The following Table 2 is an example of the data collected from the concentration of carbon dioxide released from the yeast cells with no exposure to UV. The remaining data can be found in the Appendix B (Tables B1-B15).
Table 2. Concentration of carbon dioxide released with no exposure to UV (control) without sunscreen.
Time of
recording (min) |
Concentration of carbon dioxide/ppm |
Duration of culture growth |
15 min |
30 min |
45 min |
60 min |
0 |
900 |
404 |
702 |
676 |
1.0 |
1620 |
1206 |
1024 |
1022 |
2.0 |
2118 |
1640 |
1474 |
1322 |
3.0 |
2970 |
2006 |
1786 |
1620 |
4.0 |
3574 |
2466 |
2096 |
1892 |
5.0 |
4114 |
2880 |
2464 |
2192 |
6.0 |
4624 |
3266 |
2794 |
2512 |
7.0 |
5084 |
3620 |
3126 |
2796 |
8.0 |
5604 |
3930 |
3412 |
3062 |
9.0 |
5994 |
4192 |
3644 |
3328 |
10.0 |
6520 |
4510 |
3946 |
3568 |
8. Processing of Data
In each table the rate of the change of CO2 is calculated, per time, and then the average rate is estimated together with the standard deviation values.
1) The rate is calculated with the following formula (sample calculation, Table B1, Trial 1):
2) The average rate from the five trials is calculated with the following formula (sample calculation, Table 1, Trials 1 - 5):
3) With an SD value of 94 ppm·min−1.
These results are summed up and presented in the following Table 3.
The following figure illustrates the changes in CO2 concentration with both the presence or absence of sunscreen over the yeast cells. The results presented in these tables are introduced to Excel to construct relevant graphs (Figures 4-7).
Table 3. Rate of CO2 concentration change over time in different UV exposure duration and in the presence or absence of sunscreen.
Conditions |
Rate of CO2 concentration change over time/ppm·min−1 |
Trials |
1 |
2 |
3 |
4 |
5 |
Average |
SD |
0 exposure, no sunscreen |
700 |
776 |
873 |
770 |
616 |
741 |
94 |
0 exposure, with sunscreen |
1117 |
1105 |
1239 |
1118 |
1222 |
1160 |
65 |
Before 15 min exposure no sunscreen |
531 |
520 |
476 |
455 |
485 |
493 |
32 |
After 15 min exposure no sunscreen |
154 |
156 |
141 |
129 |
142 |
145 |
11 |
Before 15 min exposure with sunscreen |
1212 |
1135 |
1166 |
1103 |
1272 |
1178 |
66 |
After 15 min exposure with sunscreen |
1158 |
956 |
1035 |
1008 |
1005 |
1032 |
76 |
Before 30 min exposure no sunscreen |
1065 |
906 |
928 |
952 |
851 |
904 |
79 |
After 30 min exposure no sunscreen |
765 |
492 |
572 |
691 |
634 |
631 |
94 |
Before 30 min exposure with sunscreen |
1343 |
1363 |
1475 |
1588 |
1477 |
1449 |
99 |
After 30 min exposure with sunscreen |
1337 |
1342 |
1377 |
1564 |
1288 |
1381 |
107 |
Before 60 min exposure no sunscreen |
702 |
637 |
599 |
495 |
473 |
581 |
97 |
After 60 min exposure no sunscreen |
483 |
471 |
415 |
398 |
549 |
462 |
60 |
Before 60 min exposure with sunscreen |
1146 |
1237 |
1311 |
1351 |
1273 |
1284 |
93 |
After 60 min exposure with sunscreen |
1328 |
1209 |
1476 |
1227 |
1288 |
1326 |
92 |
![]()
Figure 4. Concentration of carbon dioxide released with no exposure to UV (control) without sunscreen.
Figure 5. Average rate of carbon dioxide concentration change before and after exposure of yeast to UV for increasing times, with and without sunscreen (Error bars show ±1sd).
Figure 6. Average rate of carbon dioxide concentration change after exposure to UV for increasing times, with and without sunscreen (Error bars show ±1sd).
Figure 7. Cell density assessed spectrophotometrically with and without sunscreen versus times of UV exposure.
9. Statistical Analysis
1) Rate of CO2 Concentration Change:
The t-test comparing the rates of CO2 concentration change between the trials with sunscreen and without sunscreen shows that:
t-statistic: 6.577
p-value: 2.62 × 10−5
This is a very low p-value that indicates a statistically significant difference between the rates of CO2 concentration change with and without sunscreen across all exposure times.
2) Cell Density:
The t-test comparing the cell densities with sunscreen and without sunscreen shows that:
t-statistic: 0.055
p-value: 0.958
This high p-value suggests there is no statistically significant difference in cell density between the groups with and without sunscreen.
The important finding in this case is that the sunscreen appears to have a significant effect on the rate of CO2 production, but not on cell density.
3) To analyze whether there are significant differences before and after UV exposure both with and without sunscreen, separate t-tests were run for the before and after groups.
The paired t-test results comparing the rate of CO2 concentration change before and after UV exposure show the following:
Without Sunscreen:
t-statistic = 7.76
p-value = 1.94 × 10−6
This p-value is much smaller than the significance level of 0.05, indicating a statistically significant difference between the rates before and after UV exposure without sunscreen.
With sunscreen:
t-statistic = 1.81
p-value = 0.091
This p-value is larger than the significance level of 0.05, indicating no statistically significant difference between the rates before and after UV exposure with sunscreen.
In conclusion:
1) There is a significant change in the rate of CO2 concentration without sunscreen after UV exposure.
2) There is no significant change in the rate with sunscreen after UV exposure, indicating sunscreen helps decrease the adverse effect of UV on respiration rates in yeast.
10. Discussion
The observed phenomena that the cell density differences are not statistically significant, while the respiration rates are, can be explained by taking into account the effects of UV radiation on cellular metabolic processes apart from cell survival. UV radiation, mostly UVB and UVC, can cause significant damage to cellular molecules like DNA, proteins, and membranes, which would detrimentally affect the cell’s ability to function normally, even in the case that the cell survives.
1) Metabolic Machinery Damage: Although the overall number of yeast cells shown by the cell density remains intact between groups with and without sunscreen, UV radiation can damage cellular molecules essential for respiration. UV radiation causes damage to DNA, proteins, and enzymes, especially those involved in respiration like cytochrome c oxidase or enzymes in the glycolytic pathway [24]. The damage of such proteins, disrupts the electron transport chain. Thus, the cells may remain alive (thus the density remains the same), but their ability to produce ATP is compromised. Moreover, damage to mitochondria or other key organelles involved in energy production can lead to reduced metabolic efficiency [25] [26]. These damages in DNA impair the yeast cells’ ability to carry out oxidative phosphorylation, which happens in human cells, too.
2) Sublethal Damage: UV exposure may cause sublethal damage, where the yeast cells are not instantly killed but experience dysfunction. In such cases the cells may divide or survive but with impaired metabolic functions [27]. This may explain why the respiration rates are significantly lower without sunscreen, as UV-damaged cells struggle to perform effectively their cellular respiration [27] [28].
3) Heterogeneity of Damage: Not all cells may be equally influenced by UV radiation. Some cells in the population may be more resistant to UV, while others may be significantly damaged. This in turn could create a population where some cells continue to respire normally, whereas others would show severely decreased respiration, keeping the density constant but decreasing the overall CO2 production [24] [29].
4) Apoptosis or Programmed Cell Death: UV radiation may also induce apoptosis or programmed cell death mechanisms in yeast, which could result in cells that remain intact, contributing to the cell density, but being metabolically inactive, therefore contributing less to respiration. In this case, cells damaged by UV can still be detected by the spectrophotometer measuring density, but they are not functioning normally in terms of metabolism [30] [31].
5) Sunscreen Protection: Sunscreen creates protective barriers that absorb, scatter, or reflect UV radiation. The ingredients that do so may be Zinc Oxide, Titanium Dioxide, and other UV filters. This way, the UV cannot penetrate the cell membrane. This membrane can be the membrane of a yeast cell, or the cell of human skin [32].
6) Relation with Human Skin Cells: It is true that yeast cells have similarities with human skin cells. Most similarities are found in the metabolic processes that both types of cells follow. Except for metabolic processes, they follow similar division and growth processes. The similarities are the reasons that yeast cells can be a model to study human cells. But, there are also differences that cause limitations. Such differences are the process of respiration without oxygen present. Yeast cells follow alcoholic fermentation, while human cells undergo anaerobic respiration.
7) General Information: Since the role of sunscreen is so major it must be spread. Schools must implement specific sessions, not only for students, but parents as well. Another way to increase awareness, and cancer prevention, is to directly provide people with sunscreens. On the other hand, there might be a disadvantage concerning the environment. All the plastic bottles and caps, can easily be carried by wind during summer, polluting beaches and nature. This might also kill animals, distracting ecosystems [33].
By looking at the data collected we can make the following observations:
For yeast without sunscreen, the average rate of CO2 concentration did not follow a clear trend. At 0 minutes without UV exposure, the rate was 741 ppm per minute, decreasing after 15 minutes and nearly doubling at 30 minutes, indicating peak respiration. After UV exposure, respiration began later and increased more slowly, showing yeast respired faster without UV exposure.
With sunscreen, CO2 production was generally much higher, both with and without UV exposure. UV radiation slowed the onset of respiration, but CO2 production at 15, 30, and 60 minutes was consistently higher. At 60 minutes, yeast exposed to UV with sunscreen respired faster than those unexposed. The small difference in average CO2 concentration before and after exposure suggests effective protection by sunscreen. The statistical analysis supports this, with a t-statistic (6.577) and a p-value (2.62 × 10−5) confirming sunscreen’s protective role against UV-induced metabolic damage and a t-statistic (7.76) with a p-value (1.94 × 10−6) highlighting the harmful effects of UV on yeast respiration. This aligned with the hypothesis, since without sunscreen, the yeast cells’ survival decreased. This was more evident at the high exposure time (60 minutes). On the other hand, in the presence of sunscreen most yeast cells survived, with the rate of respiration increasing.
In conclusion, this study highlights the significant protective role of sunscreen in mitigating the adverse effects of UV radiation on Saccharomyces cerevisiae, a eukaryotic model organism. By preserving metabolic processes and shielding cells from UV-induced damage, sunscreen proves critical in protecting cellular components essential for survival. Furthermore, the findings establish a clear link between UV exposure and metabolic dysfunction, reinforcing the parallels between yeast and human skin cells and emphasizing sunscreen’s importance in promoting cellular health and preventing damage.
11. Evaluation
In Table 4, the limitations of the experiment and ways to improve such problems are suggested.
Table 4. Evaluation of data collected.
Limitations |
Suggested improvements |
In the control runs, the water bath was used to match the yeast solution’s temperature to the ambient temperature of the other samples. However, some flasks remained in the water bath longer, causing temperature variations that could have affected the cells differently. |
To improve this, each trial should be carried out on its own, placing only one flask within the water bath and removing it at the appropriate time. |
The effects of UV radiation were examined on only one type of yeast, dry yeast. |
To improve this, repeat the procedure using wet yeast, to collect comparable data. |
The location where the flasks were placed was not kept constant, due to the absence
or presence of sunlight on each particular day. |
A solution of this would be to place them in the UV chamber, so that they receive the same amount of radiation, however it would only be UVC. |
The UV intensity varied from day to day due to the presence of clouds. (Figure A3, Appendix A) |
Yeasts should be placed in the UV chamber, so that they receive the same amount of radiation, however it would only be UVC. |
The magnetic stirrer was not on operation while the data was being collected. |
To improve this, leave the magnetic stirrer on during the entire duration of data collection. |
The flasks were left outdoors for a longer period of time than others, thus receiving more UV radiation. |
To improve this, each trial should be carried out on its own, placing only one flask outdoors at each time. |
Some specimens of yeast were not
measured directly after the appropriate
time of exposure to UV radiation, and
were left indoors for some period of time. |
To improve this, set up more than one stations, or carry out a larger number of trials, for example 10 trials, so as to collect more sufficient data. |
Appendix A
Table A1. Chemical composition of Frezyderm seaside sunscreen UV protection level 50+ [22].
Ingredient name |
Purpose |
Wavelength protection |
C13-15 alkane |
Solvent, emollient |
- |
Ethylhexyl Methoxycinnamate |
sunscreen |
UVB [34] |
Dibutyl adipate |
Emollient, solvent |
|
Diethylamino hydroxybenzyl Hexyl benzoate |
sunscreen |
UVA [35] |
Octocrylene |
sunscreen |
UVA, UVB [36] |
Ethylhexyl salicylate |
sunscreen |
UVB [37] |
Butyl methoxydibenzoylmethane |
sunscreen |
UVA [38] |
Perfume |
Perfuming |
- |
Benzyl alcohol |
Preservation, perfuming, solvent, viscosity, controlling |
- |
Figure A1. Relative humidity during 2 June-30 June 2024, when I carried out the experiment.
Figure A2. Maximum temperature measurements during 2 June-30 June 2024, when I carried out my experiment.
Figure A3. UV index during 2 June-30 June 2024, when I carried out my experiment.
Appendix B
Table B1. Concentration of carbon dioxide released at 0 min exposure without sunscreen.
Control |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
528 |
922 |
582 |
826 |
956 |
1.0 |
1686 |
2214 |
1794 |
1774 |
1770 |
2.0 |
2488 |
3290 |
3032 |
2864 |
2740 |
3.0 |
3332 |
4232 |
4118 |
3814 |
3532 |
4.0 |
4058 |
4976 |
4980 |
4598 |
4194 |
5.0 |
4706 |
5788 |
5842 |
5408 |
4750 |
6.0 |
5334 |
6478 |
6648 |
6200 |
5300 |
7.0 |
5962 |
7074 |
7414 |
6892 |
5792 |
8.0 |
6532 |
7612 |
8100 |
7480 |
6216 |
9.0 |
7058 |
8092 |
8744 |
8000 |
6610 |
10.0 |
7526 |
8682 |
9316 |
8522 |
7116 |
Table B2. Concentration of carbon dioxide released at 0 min exposure with sunscreen.
Control |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
1238 |
1208 |
4244 |
1776 |
4496 |
1.0 |
1980 |
2052 |
5370 |
1818 |
5482 |
2.0 |
3442 |
3642 |
6026 |
3106 |
6462 |
3.0 |
4716 |
4924 |
7704 |
4410 |
8060 |
4.0 |
6124 |
6248 |
9172 |
5620 |
10,064 |
5.0 |
7350 |
7360 |
11,366 |
7006 |
11,920 |
6.0 |
8488 |
8402 |
13,072 |
8364 |
13,354 |
7.0 |
9492 |
9352 |
14,386 |
9556 |
14,502 |
8.0 |
10,472 |
10,196 |
15,294 |
10,734 |
15,516 |
9.0 |
11,482 |
11,136 |
16,034 |
11,764 |
16,214 |
10.0 |
12,406 |
12,260 |
16,632 |
12,956 |
16,718 |
Table B3. Concentration of carbon dioxide released before 15 min exposure without sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
528 |
982 |
664 |
742 |
846 |
1.0 |
1200 |
1346 |
1192 |
1012 |
1190 |
2.0 |
1608 |
1748 |
1532 |
1354 |
1576 |
3.0 |
2158 |
2214 |
2028 |
1868 |
1990 |
4.0 |
2782 |
2860 |
2596 |
2416 |
2588 |
5.0 |
3364 |
3492 |
3096 |
2934 |
3182 |
6.0 |
3916 |
4086 |
3560 |
3430 |
3738 |
7.0 |
4456 |
4650 |
4082 |
3922 |
4284 |
8.0 |
4940 |
5188 |
4560 |
4398 |
4786 |
9.0 |
5408 |
5692 |
5004 |
4854 |
5264 |
10.0 |
5842 |
6178 |
5426 |
5288 |
5700 |
Table B4. Concentration of carbon dioxide released after 15 min exposure without sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
500 |
600 |
550 |
480 |
510 |
1.0 |
764 |
854 |
792 |
728 |
770 |
2.0 |
814 |
902 |
840 |
780 |
818 |
3.0 |
844 |
934 |
872 |
812 |
848 |
4.0 |
874 |
966 |
904 |
838 |
872 |
5.0 |
898 |
992 |
926 |
864 |
894 |
6.0 |
926 |
1012 |
950 |
888 |
918 |
7.0 |
1096 |
1194 |
1064 |
994 |
1040 |
8.0 |
1432 |
1504 |
1348 |
1240 |
1344 |
9.0 |
1738 |
1816 |
1654 |
1502 |
1648 |
10.0 |
2044 |
2156 |
1964 |
1774 |
1934 |
Table B5. Concentration of carbon dioxide released before 15 min exposure with sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
564 |
1012 |
944 |
550 |
3538 |
1.0 |
912 |
1532 |
1572 |
1200 |
4372 |
2.0 |
1562 |
2340 |
3058 |
2954 |
5470 |
3.0 |
2328 |
4144 |
4386 |
3030 |
6506 |
4.0 |
3194 |
5282 |
5654 |
4240 |
8230 |
5.0 |
4970 |
6596 |
6954 |
5500 |
9836 |
6.0 |
5682 |
7642 |
8118 |
6768 |
11,550 |
7.0 |
6430 |
8618 |
9294 |
7922 |
13,072 |
8.0 |
7212 |
9526 |
10,428 |
8066 |
14,348 |
9.0 |
9970 |
10,380 |
11,570 |
9504 |
15,388 |
10.0 |
12,688 |
12,366 |
12,602 |
11,586 |
16,260 |
Table B6. Concentration of carbon dioxide released after 15 min exposure with sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
1318 |
1030 |
1132 |
1024 |
1262 |
1.0 |
2416 |
1832 |
2156 |
2394 |
2250 |
2.0 |
4136 |
2878 |
3654 |
3800 |
3806 |
3.0 |
5838 |
4026 |
4966 |
4972 |
5218 |
4.0 |
7326 |
5206 |
6326 |
6196 |
6572 |
5.0 |
8512 |
6428 |
7450 |
7266 |
7622 |
6.0 |
9526 |
7454 |
8350 |
8214 |
8532 |
7.0 |
10,534 |
8360 |
9220 |
9098 |
9330 |
8.0 |
11,430 |
9160 |
9966 |
9784 |
10,000 |
9.0 |
12,240 |
9828 |
10,762 |
10,442 |
10,712 |
10.0 |
12,900 |
10,590 |
11,486 |
11,106 |
11,308 |
Table B7. Concentration of carbon dioxide released before 30 min exposure without sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
1740 |
1694 |
1756 |
1588 |
878 |
1.0 |
2922 |
2890 |
2744 |
2954 |
1652 |
2.0 |
5354 |
4696 |
4818 |
4736 |
3346 |
3.0 |
7164 |
6158 |
6356 |
6250 |
4680 |
4.0 |
8394 |
7216 |
7472 |
7412 |
5734 |
5.0 |
9208 |
8006 |
8268 |
8266 |
6582 |
6.0 |
9824 |
8680 |
8884 |
8946 |
7250 |
7.0 |
10,510 |
9224 |
9432 |
9502 |
7800 |
8.0 |
11,234 |
9728 |
9916 |
9986 |
8346 |
9.0 |
11,878 |
10,246 |
10,488 |
10,566 |
8896 |
10.0 |
12,390 |
10,756 |
11,036 |
11,108 |
9386 |
Table B8. Concentration of carbon dioxide released after 30 min exposure without sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
500 |
1544 |
1342 |
938 |
916 |
1.0 |
2298 |
1124 |
1816 |
1956 |
2210 |
2.0 |
3926 |
1108 |
3102 |
3478 |
3454 |
3.0 |
4910 |
1780 |
4096 |
4474 |
4342 |
4.0 |
5714 |
2974 |
4746 |
5196 |
4952 |
5.0 |
6254 |
3938 |
5272 |
5874 |
5486 |
6.0 |
6558 |
4620 |
5766 |
6384 |
5908 |
7.0 |
6980 |
5162 |
6122 |
6828 |
6272 |
8.0 |
7414 |
5672 |
6464 |
7212 |
6622 |
9.0 |
7798 |
6092 |
6792 |
7540 |
6968 |
10.0 |
8148 |
6466 |
7060 |
7844 |
7256 |
Table B9. Concentration of carbon dioxide released before 30 min exposure with sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
1686 |
1478 |
1936 |
5874 |
4380 |
1.0 |
2210 |
2806 |
2178 |
7342 |
5228 |
2.0 |
4642 |
4328 |
4864 |
8668 |
6516 |
3.0 |
6900 |
5832 |
7210 |
9600 |
8764 |
4.0 |
8662 |
7340 |
8956 |
12,518 |
9714 |
5.0 |
10,116 |
8688 |
10,296 |
14,824 |
12,776 |
6.0 |
11,616 |
9844 |
11,616 |
16,546 |
14,502 |
7.0 |
12,770 |
11,148 |
13,620 |
17,876 |
15,776 |
8.0 |
13,682 |
12,360 |
14,400 |
18,930 |
17,120 |
9.0 |
14,440 |
14,278 |
15,060 |
19,814 |
18,112 |
10.0 |
15,120 |
15,106 |
16,690 |
21,750 |
19,152 |
Table B10. Concentration of carbon dioxide released after 30 min exposure with sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
2350 |
2662 |
2420 |
2440 |
3400 |
1.0 |
3298 |
3560 |
3812 |
3748 |
4102 |
2.0 |
4564 |
4889 |
5186 |
5772 |
5606 |
3.0 |
6090 |
6410 |
6930 |
8250 |
6898 |
4.0 |
7744 |
8054 |
8542 |
10,900 |
8994 |
5.0 |
9442 |
9762 |
10,266 |
12,820 |
10,854 |
6.0 |
11,036 |
11,290 |
11,562 |
14,354 |
12,466 |
7.0 |
12,450 |
12,778 |
12,820 |
15,586 |
13,640 |
8.0 |
13,710 |
13,050 |
13,980 |
16,540 |
14,672 |
9.0 |
14,784 |
15,043 |
15,106 |
17,264 |
15,510 |
10.0 |
15,720 |
16,080 |
16,182 |
18,080 |
16,284 |
Table B11. Concentration of carbon dioxide released before 60 min exposure without sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
640 |
1274 |
724 |
696 |
814 |
1.0 |
1476 |
1894 |
1144 |
1066 |
1066 |
2.0 |
2180 |
2690 |
1866 |
1574 |
1486 |
3.0 |
3148 |
3476 |
2682 |
2132 |
1946 |
4.0 |
3940 |
4202 |
3412 |
2782 |
2534 |
5.0 |
4630 |
4872 |
4050 |
3344 |
3116 |
6.0 |
5300 |
5564 |
4614 |
3862 |
3634 |
7.0 |
5992 |
6184 |
5160 |
4352 |
4138 |
8.0 |
6604 |
6726 |
5740 |
4790 |
4594 |
9.0 |
7160 |
7212 |
6254 |
5202 |
5034 |
10.0 |
7660 |
7648 |
6710 |
5644 |
5542 |
Table B12. Concentration of carbon dioxide released after 60 min exposure without sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
500 |
438 |
622 |
1288 |
810 |
1.0 |
1124 |
1032 |
894 |
1714 |
972 |
2.0 |
1758 |
1572 |
1320 |
2256 |
1728 |
3.0 |
2392 |
2032 |
1834 |
2796 |
2502 |
4.0 |
2984 |
2604 |
2376 |
3276 |
3256 |
5.0 |
3444 |
3130 |
2892 |
3732 |
3880 |
6.0 |
3904 |
3606 |
3336 |
4120 |
4436 |
7.0 |
4310 |
4050 |
3758 |
4476 |
4948 |
8.0 |
4674 |
4420 |
4122 |
4796 |
5502 |
9.0 |
5002 |
4776 |
4462 |
5122 |
6028 |
10.0 |
5332 |
5146 |
4770 |
5268 |
6302 |
Table B13. Concentration of carbon dioxide released before 60 min exposure with sunscreen.
Before |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
530 |
550 |
1144 |
1828 |
2374 |
1.0 |
1314 |
1740 |
2092 |
2370 |
2808 |
2.0 |
2118 |
3660 |
4198 |
4464 |
5472 |
3.0 |
3172 |
5262 |
5898 |
6792 |
7858 |
4.0 |
4244 |
6622 |
7478 |
8650 |
9722 |
5.0 |
5256 |
7746 |
8892 |
10,236 |
11,364 |
6.0 |
6334 |
8824 |
10,072 |
11,778 |
12,892 |
7.0 |
7232 |
9962 |
11,368 |
12,884 |
14,054 |
8.0 |
8074 |
10,886 |
12,468 |
13,804 |
14,926 |
9.0 |
9844 |
11,812 |
13,336 |
14,658 |
15,808 |
10.0 |
11,992 |
12,916 |
14,250 |
15,334 |
16,116 |
Table B14. Concentration of carbon dioxide released after 60 min exposure with sunscreen.
After |
Concentration of carbon dioxide/ppm |
Time (min) |
Trial 1 |
Trial 2 |
Trial 3 |
Trial 4 |
Trial 5 |
0 |
6582 |
5422 |
2572 |
4608 |
1856 |
1.0 |
7268 |
6076 |
4882 |
6558 |
3824 |
2.0 |
8174 |
7160 |
8042 |
7938 |
6270 |
3.0 |
9784 |
9622 |
10,640 |
10,118 |
8160 |
4.0 |
12,730 |
11,854 |
12,666 |
12,212 |
9712 |
5.0 |
12,750 |
13,712 |
14,166 |
13,766 |
11,164 |
6.0 |
16,206 |
15,088 |
15,162 |
14,774 |
12,392 |
7.0 |
17,444 |
16,132 |
15,972 |
15,464 |
13,334 |
8.0 |
18,432 |
17,036 |
16,648 |
16,118 |
13,902 |
9.0 |
19,204 |
17,870 |
16,994 |
16,468 |
14,314 |
10.0 |
19,869 |
18,508 |
17,328 |
16,882 |
14,738 |
Table B15. Cell density with and without sunscreen for each exposure time.
Before exposure: N = 18.92 × 10−4 |
Time of exposure in UV (min) |
With sunscreen (9.0 ml/50) |
Without sunscreen |
Control |
12.73 × 10−4 |
12.5 × 10−4 |
15 |
15.5 × 10−4 |
15.86 × 10−4 |
30 |
18.08 × 10−4 |
24.24 × 10−4 |
60 |
11.71 × 10−4 |
4.46 × 10−4 |