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Effect Of Subacute Selenium Poisoning On Reproduction And Immunity Of Male Mice

Posted on:2013-04-08Degree:MasterType:Thesis
Country:ChinaCandidate:Y J GuanFull Text:PDF
GTID:2233330377457861Subject:Clinical Veterinary Medicine
Abstract/Summary:PDF Full Text Request
In this experiment the healthy male Kunming mice was the object of study.. Four dose groups were set:control group (0.00mg/kg), sodium selenite low dose group (1/80LD50,0.14mg/kg), middle dose group (1/20LD50,0.54mg/kg) and high dose group (1/5LD5O,2.16mg/kg). The mice were intragastrically exposed sodium selenite at the same tine every morning, which continued for30days. After being exposed selenite for10,20or30days, the mice were killed with the method of cervical dislocation. The testis, thymus and spleen were taken quickly. They were disposed and conserved according to different need. The detection of organ coefficient of testis, thymus and spleen, histological structure of testis and spleen, sperm motility and density, sperm deformity rate, energy metabolism and antioxidant capacity of testis and spleen, the content of selenium in spleen, the phagocytosis of peritoneal macrophage, the level of antibody forming cell in spleen and T-lymphocyte in the peripheral blood were used to study the toxic effect of subacute selenite poisoning on the reproductive system and immune system of mice. The results showed as follow:The organ coefficient of mice testis, spleen and thymus decreased and the normal growth and development of organs were destroyed after having been exposed selenite.The detective results of sperm motility, density and deformity rate showed sperm motility and density apparently decreased and the deformity rate significantly increased, which confirmed subacute selenite poisoning could damage the production and development of sperm and lead to sperm distortion.Observation of testicular histological structure showed subacute selenite poisoning could disrupt normal testicular anatomical structure and cause the seminiferous tubule degenerate and seminiferous duct wall get thinner and even rupture. It also caused testicular interstitial cell degeneration necrosis and then affected the normal testicular spermatogenic ability and endocrine function.Testicular lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) content were detected with kit. The results showed testicular energy metabolism and antioxidant capacity were impaired, oxidative stress was induced and energy supply was not enough, all of which caused the decline of testicular spermatogenic ability.The detection of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), total antioxidant capacity (T-AOC), and the content of malondialdehyde (MDA) and selenium in spleen showed antioxidant ability of spleen dereased and oxidative damage had occurred. The increase of GSH-Px activity and spleen selenium content showed the seleniun produced accumulative toxicity to spleen.The detection of the phagocytosis of peritoneal macrophage, the level of antibody forming cell in spleen and T-lymphocyte in the peripheral blood showed subacute selenite poisoning could respectively inhibite non-specific immunity, humoral immunity and cell immunity and then inhibite immune level of body.In conclusion subacute selenite poisoning could inhibit growth and development of reproductive and immune organ, destroy their normal structures, damage the antioxidant system, inhibit phagocytic function of macrophage, reduced the level of antibody forming cell in spleen and T-lymphocyte in the peripheral blood. This experiment systematically studied the toxicity effect of subacute selenite poisoning on the reproduction and immune system of mice from the level of organ, cellular, subcellular, confirmed the two-way adjusting effect of selenite on reproductive and immune function of mice, enriched the knowledge in toxicology and provided a scientific basis for clinical supplement of selenium.
Keywords/Search Tags:sodiurn selenite, ultrathin section, macrophagocyte, acidalpha naphthyl aetate esterase, hemolytic plaque
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