The ACE D/I and PAI-1 4G/5G gene polymorphisms might represent risk factor in PCOS with SAB. Homozygosity for ACE D or PAI-1 4G polymorphisms as well as compound carrier status are significant positive explanatory variable for PCOS patients with SAB, which may result in increased PAI-1 concentrations and hypofibrinolysis and contribute to early pregnancy loss.

Our results raise the possibility that MMPs may be implicated in the pathophysiology of PCOS either by regulating ovarian tissue remodeling or indirectly by facilitating IGF-I bioavailability through proteolysis of IGFBP-1.

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Uncoupling protein 2 (UCP 2 ), an inner mitochondrial membrane protein, can limit the generation of reactive oxygen species (ROS) and protect cells from injuries mediated by oxidative stress. We investigated the effect of upregulation of UCP 2 in the regenerating liver 96 h after 68% partial hepatectomy (PH) on the self-protection of regenerating liver against carbon tetrachloride (CCl 4 ) poisoning. Hepatotoxicity was induced in vivo by administering CCl 4 to rats that had undergone PH. After CCl 4 poisoning, the regenerating liver appeared to have less histological damage and lower serum alanine aminotransferase (ALT) levels. Lower malondialdehyde production and higher glutathione contents were also observed in the regenerating liver compared with the shamoperated liver after CCl 4 poisoning. UCP 2 expression was markedly elevated in the regenerating liver, and further increased after CCl 4 intoxication. Mitochondrial membrane potential and adenosine triphosphate stores maintained higher levels in the regenerating liver than in sham-operated liver after CCl 4 intoxication. The results showed that the regenerating liver exhibited a potent ability to resist CCl 4 intoxication, and the autoprotection of regenerating liver might result from reduction of ROS by UCP 2 and maintenance of higher ATP stores.