Molecular mechanisms of Cisplatin (cas 15663-27-1)- induced placental toxicity and teratogenicity in rats and the ameliorating role of N-acetyl-cysteine

Add time:09/01/2019    Source:sciencedirect.com

The aim of the present study is to investigate the molecular mechanisms of Cisplatin- induced placental toxicity and teratogenicity in rats and the ameliorating role of N-acetyl-cysteine (NAC). Cisplatin was administrated intraperitoneally at 5 mg/kg.b.wt as a single dose on the 12th day of gestation while NAC was administered orally throughout gestation either alone or in concomitant injection of Cisplatin at 200 mg/kg.b.wt. Cisplatin + NAC group showed reduction in the elevated morphological, visceral and skeletal abnormalities as well as the morphological and histopathological changes in placenta compared to Cisplatin - treated rats. Importantly, NAC attenuated Cisplatin-induced placental apoptosis through down-regulation of Fas and Caspase-3 genes expression. In conclusion, induction of placental apoptosis by overexpression of Fas and Caspase-3 genes gives a new insight into the mechanism of Cisplatin teratogenicity. The protective role of NAC, on the other hand, was characterized by attenuation of Fas and Caspase-3 genes- mediated apoptosis.

We also recommend Trading Suppliers and Manufacturers of Cisplatin (cas 15663-27-1). Pls Click Website Link as below: cas 15663-27-1 suppliers

Prev:Molecules in focusRYANODINE (cas 15662-33-6) receptor Ca2+ release channel post-translational modification: Central player in cardiac and skeletal muscle disease
Next:Sodium Pheophorbide A (cas 15664-29-6) has photoactivated fungicidal activity against Pestalotiopsis neglecta)