title: Low selenium diet alters cell cycle phase, apoptotic population and modifies oxidative stress markers of spleens in broilers.
abstract: The purpose of this 42-day study was to investigate the effects of low selenium (Se) on histopathological changes of spleen, cell cycle and apoptosis of splenocytes, and oxidative status of the spleen. One hundred twenty 1-day-old avian broilers were randomly divided into two groups of 60 each and were fed on a low Se diet (0.0342 mg/kg Se) or a control diet (0.2 mg/kg Se), respectively. The weight and relative weight of the spleen were significantly decreased in the low Se group when compared with those of the control group. Histopathologically, splenic lesions in low-Se chicken were characterized by lymphocyte depletion and congestion of red pulp. As measured by flow cytometry, splenocytes in G(0)/G(1) phase were significantly increased, while splenocytes in S phase and G(2) + M phase were obviously decreased in the low Se group. The percentage of apoptotic splenocytes was greatly increased in the low Se group when compared with that of control group. At the same time, the occurrence frequencies of apoptotic splenocytes was markedly increased in the low Se group with the appearance of condensed nucleus ultrastructurally. Oxidative stress in the spleens of the low Se group was evidenced by decrease in glutathione peroxidase and catalase activities and increase in malondialdehyde contents. The results showed that low Se diet intake caused increased apoptosis, arrested cell cycle, and obvious oxidative stress, which provided a possible pathway for the injured structure and immune function of the spleen in chickens.
authors.affiliation: College of Veterinary Medicine, Sichuan Agricultural University, Ya'an, Sichuan, China 625014.
authors.forename: Xi
authors.initials: X
authors.lastname: Peng
authors.forename: Hengmin
authors.initials: H
authors.lastname: Cui
authors.forename: Jing
authors.initials: J
authors.lastname: Fang
authors.forename: Zhicai
authors.initials: Z
authors.lastname: Zuo
authors.forename: Junliang
authors.initials: J
authors.lastname: Deng
authors.forename: Kangcheng
authors.initials: K
authors.lastname: Pan
authors.forename: Weimin
authors.initials: W
authors.lastname: Lai
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhou
mesh_terms: D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002453:Cell Cycle / Q000187:drug effects*; D002467:Cell Nucleus / Q000378:metabolism / Q000648:ultrastructure; D002645:Chickens / Q000378:metabolism; D004032:Diet; D004789:Enzyme Activation; D005434:Flow Cytometry; D005979:Glutathione Peroxidase / Q000378:metabolism; D008214:Lymphocytes / Q000473:pathology; D008315:Malondialdehyde / Q000378:metabolism; D009929:Organ Size; D018384:Oxidative Stress; D012643:Selenium / Q000172:deficiency* / Q000494:pharmacology; D013154:Spleen / Q000187:drug effects / Q000201:enzymology / Q000473:pathology*
chemical_list: D015415:Biomarkers; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D012643:Selenium