Pathology of spleen in chickens fed on a diet deficient in methionine
Bangyuan Wu, Hengmin Cui, Xi Peng, Jing Fang, Wei Cui, Xiaodong Liu
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DOI: 10.4236/health.2012.41007   PDF    HTML     5,396 Downloads   9,455 Views   Citations

Abstract

The purpose of this 42-day study was to investigate the effects of methionine deficiency on spleen by determining the relative weight, morphological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative markers of serum and spleen. One hundred and twenty one-day-old avian broilers were randomly divided into two groups and fed on a control diet (starter diet, methionine 0.50%; grower diet, methionine 0.40%) and methionine deficient diet (starter diet, methionine 0.26%; grower diet, methionine 0.28%) for 6 weeks. The relative weight of spleen was lighter in methionine deficiency than control group. Histopathologically, lymphopenia and congestion were observed. Ultrastructurally, there were more apoptosis lymphocytes in spleen and the mitochondria of lymphocytes were swelled in methionine deficiency. By flow cytometry, the G0/G1 phase of the cell cycle of the spleen was much higher (P < 0.01), and the S, G2+M phases and proliferating index were lower (P < 0.01) in methionine deficiency than in control group. And the percentage of apoptotic cells in the spleen was significantly increased in methionine deficiency (P < 0.01).The superoxide dismutase and glutathione peroxidase activities, and abilities to inhibit hydroxyl radicals were greatly decreased while the malondialdehyde contents were markedly increased in methionine deficiency. It was concluded that methionine deficiency could restraine the development of the spleen by cell cycle arrest and increased apoptosis, cause splenic lesions and reduce splenic antioxidant function. The splenic function should be finally impaired and then the immune function could be impacted in chickens.

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Wu, B. , Cui, H. , Peng, X. , Fang, J. , Cui, W. and Liu, X. (2012) Pathology of spleen in chickens fed on a diet deficient in methionine. Health, 4, 32-38. doi: 10.4236/health.2012.41007.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Carew, L.B., McMurtry J.P. and Alster, F.A. (2003) Effects of methionine deficiencies on plasma levels of thyroid hormones, insulin-like Growth Factors-I and -II, Liver and Body Weights and Feed Intake in Growing Chickens. Poultry Science, 82, 1932-1938.
[2] Cummins, A.G., Bolin, T.D., Duncombe, V.M. and Davis, A.E. (1986) The effect of methionine and protein deficiency in delaying expulsion of Nippostrongylus brasiliensis in the rat. The American Journal Clinical Nutrition, 44, 857-862.
[3] Dunlevy, L.P.E., Burren, K.A., Chitty, L.S., Copp, A.J. and Greene, N.D.E. (2006) Excess methionine suppresses the methylation cycle and inhibits neural tube closure in mouse embryos. FEBS Letters, 11, 2803-2807. doi:10.1016/j.febslet.2006.04.020
[4] Kano, Y., Sakamoto, S., Kasahara, T., Kusumoto, K., Hida, K., Suda, K., Ozawa, K., Miura, Y. and Takaku, F. (1982) Methionine dependency of cell growth in normal and malignant hematopoietic cells. Cancer Research, 42, 3090-3092.
[5] Cummins, A.G., Duncombe, V.M., Bolin, T.D. and Davis, A.E. (1985) Reversible nutritional myopathy with myotonia in the protein-deficient rat given methionine. Australian Journal Experimental Biology and Medical Science, 63, l27-137.
[6] Mori, N. and Hirayama, K. (2000) Long-term consumption of a methionine-supplemented diet increases iron and lipid peroxide levels in rat liver. The Journal of Nutrition, 130, 2349-2355.
[7] Feo, F., Pascale, R., Garcea, R., Daino, L., Pirisi, L., Frassetto, S., Ruggiu, M.E., Di Padova, C. and Stramentinoli, G. (1986) Effect of the variations of S-adeno-syl-L-methionine liver content on fat accumulation and ethanol metabolism in ethanol-intoxicated rats. Toxicology and Applied Pharmacology, 2, 331-341. doi:10.1016/0041-008X(86)90310-8
[8] Swain, B.K. and Johri, T.S. (2000) Effect of supplemental methionine, choline and their combinations on the performance and immune response of broilers. British Poultry Science, 41, 83-88. doi:10.1080/00071660086457
[9] Tsiagbe, V.K., Cook, M.E., Harper, A.E. and Sunde, M.L. (1987a) Enhanced immune responses in broiler chicks fed methionine-supplemented diets. Poultry Science, 66, 1147-1154.
[10] Tsiagbe, V.K., Cook, M.E., Harper, A.E. and Sunde, M.L. (1987) Efficacy of cysteine in replacing methionine in the immune responses of broiler chicks. Poultry Science, 66, 1138-1146.
[11] Klasing, K.C. and Barnes, D.M. (1988) Decreased amino acid requirements of growing chicks due to immunologic stress. The Journal of Nutrition, 118, 1158-1164.
[12] Konashi, S., Takahashi, K. and Akiba, Y. (2000) Effects of dietary essential amino acid deficiencies on immunological variables in broiler chickens. British Journal of Nutrition, 83, 449-456.
[13] Yen, C.L.E, Mar, M.H., Craciunescu, C.N., Edwards, L.J. and Zeisel, S.H. (2002) Deficiency in Methionine, Tryptophan, Isoleucine, or Choline Induces Apoptosis in Cultured Cells. The Journal of Nutrition, 132, 1840-1847.
[14] Benevenga, N.J. (1974) Toxicities of methionine and other amino acids. Journal of Agricultural and Food Chemistry, 22, 2-9. doi:10.1021/jf60191a036
[15] Benevenga, N.J. and Steele, R.D. (1984) Adverse effects of excessive consumption of amino acids. Annual Review of Nutrition, 4, 157-181. doi:10.1146/annurev.nu.04.070184.001105
[16] Cui, H.M., Fang, J. and Peng, X. (2003) Pathology of the thymus, spleen and bursa of Fabricius in zinc-deficient ducklings. Avian Pathology, 32, 259-263. doi:10.1080/10307945031000097840
[17] Peng, X., Cui, Y., Cui, W., Deng, J.L. and Cui, H.M. (2009) The decrease of relative weight, lesions, and apoptosis of Bursa of Fabricius induced by excess dietary selenium in chickens. Biological Trace Element Research, 131, 33-42. doi:10.1007/s12011-009-8345-6
[18] Bradford, M.M. (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Analytical Biochemistry, 72, 248-254. doi:10.1016/0003-2697(76)90527-3
[19] Pines, J. (1995) Cyclins, CDKs and cancer. Seminars Cancer Biology, 6, 63-72. doi:10.1006/scbi.1995.0009
[20] Bonham, M., O’Connor, J.M., Hannigan, B.M. and Strain JJ. (2002) The immune system as a physiological indicator of marginal copper status. British Journal of Nutrition, 87, 383-403. doi:10.1079/BJN2002558
[21] Palmer, A.M., Greengrass, P.M. snd Cavalla, D. (2000) The role of mitochondria in apoptosis. Drug News Perspect, 13, 378-384.
[22] Raisbeck, M.F., Siemion, R.S. and Smith, M.A. (2006) Modest copper supplementation blocks molybdenosis in cattle. Journal of Veterinary Diagnostic Invest, 18, 566-572. doi:10.1177/104063870601800607
[23] Halliwell, B. and Chirico, S. (1993) Lipid peroxidation: its mechanism, measurement, and significance. The American Journal Clinical Nutrition, 57, 715S-725S.
[24] Reed, D.J. and Orrenius, S. (1977) The role of methionine in glutathione biosynthesis by isolated hepatocytes. Biochemical and Biophysical Research Communications, 77, 1257-1264. doi:10.1016/S0006-291X(77)80115-0
[25] Reed, D.J. (1990) Glutathione: toxicological implications. Annual Review Pharmacology and Toxicology, 30, 603-631. doi:10.1146/annurev.pa.30.040190.003131
[26] Meister, A. (1981) On the cycles of glutathione metabolism and transport. Current Topics Cell Regulation, 18, 21-58.

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