Mitochondrial energy metabolism dysfunction involved in reproductive toxicity of mice caused by endosulfan and protective effects of vitamin E.
The experiment was designed to study the mechanism of reproductive toxicity caused by endosulfan in mice and protective effects of vitamin E. The experiment was composed of three groups: the control group did not receive any endosulfan and vitamin E; the endosulfan exposed group received 0.8 mg/kg/d endosulfan and 0mg/kg/d vitamin E; and the endosulfan+vitamin E group received 0.8 mg/kg/d endosulfan and 100mg/kg/d vitamin E. The results showed that vitamin E significantly reversed the decline of the concentration and motility rate of sperm, and inhibited the increase of sperm abnormality rate caused by endosulfan. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and lactate dehydrogenase-C4 (LDH-C4) and the level of adenosine triphosphate (ATP) in the endosulfan+vitamin E group were higher while the malondialdehyde (MDA) content was significantly lower than those of the endosulfan exposed group. The results from pathology and electron microscope observed showed vitamin E decreased the cavities formation by desquamating of spermatogenic cells, stopped the ruptures and disappearances of mitochondrial cristaes in spermatogenic cells, and prevented the breakages and partial dissolvings of sperm tails induced by endosulfan. It is likely that endosulfan could directly damage sperm structures by oxidative stress, leading to a decrease in sperm quantity and quality. It also could indirectly cause a decline in reproductive function by damaging the structure of mitochondria, resulting in energy metabolism dysfunction, which could be one of the mechanisms behind the reproductive toxicity induced by endosulfan. It was inferred that vitamin E helps maintain the structural integrities of sperm architecture and prevent mitochondrial dysfunction through inhibiting oxidative stress, and thereby prevent the reproductive dysfunctions caused by endosulfan.
Department of Laboratory Animal Science, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Na
N
Wang
Hong-Yan
HY
Qian
Xian-Qing
XQ
Zhou
Yan-Bo
YB
Li
Zhi-Wei
ZW
Sun
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D004726:Endosulfan / Q000633:toxicity*; D004734:Energy Metabolism / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D007306:Insecticides / Q000633:toxicity*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D011897:Random Allocation; D012098:Reproduction / Q000187:drug effects; D013094:Spermatozoa / Q000187:drug effects; D013737:Testis / Q000187:drug effects / Q000201:enzymology / Q000648:ultrastructure; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D007306:Insecticides; D014810:Vitamin E; D008315:Malondialdehyde; D000255:Adenosine Triphosphate; D004726:Endosulfan