Bee honey and Nigella sativa inhibit nitric oxide mediated cytochrome C release and down regulation of connexin 43 induced by methylnitrosourea in hepatic tissues of Sprague Dawley rats

We investigated the protective effect of bee honey and Nigella sativa against methylnitrosourea [MNU] induced oxidative stress, apoptosis and down-regulation of the gap junction protein connexin 43 [Cx43] in hepatic tissues. Our results showed that MNU induced hepatic dysplasia and oxidative stress through decreasing reduced glutathione [GSH] level, decreasing the activities of glutathione reductase [GRase] and superoxide dismutase [SOD], enhancing glutathione peroxidase [GPx] activity and elevating nitric oxide [NO] level in liver tissues as compared to control. Apoptosis, as indicated by significant release of cytochrome c [cyto c] from mitochondria into the cytosol, was observed in MNU injected rats and was positively correlated with the elevation of N0 level. Bee honey and Nigella protected against the previous deleterious changes by significant elevation of GSH level, increasing the activities of GRase and SOD, decreasing the activity of GPx, decreasing NO level and stopping release of cyto c from mitochondria as compared to MNU injected rats. Moreover, down-regulation of Cx43 by MNU was prevented in 50% and 75% of animals that received Nigella alone or both Nigella and bee honey, respectively. These data illustrated the consequences of MNU induced hepatocellular dysplastic changes and oxidative stress and shed the light about the possible sites targeted by bee honey and Nigella in their protective effect against the earlier stages of liver carcinogenesis

Arylesterase and paraoxonase in serum and liver of mice infected with Schistosoma mansoni: effect of zinc administration

This study aimed to evaluate the activities of arylesterase and paraoxonase in serum and liver as well as arylesterase isoenzymes in mice infected with S. mansoni. Also the degree of liver damage and the effect of dietary administration of zinc have been evaluated. Ninety mice were divided into two major groups: group [I], [30 mice] serve as control, 15 mice each fed on either standard diet, group [la], or supplemented with zinc, group [lb]; group [II], 60 infected mice with cercariae of S. mansoni, 30 mice each fed on either standard diet, group [Ila], or supplemented with zinc group [Ilb]. Blood samples and liver were collected from five animals of group la and lb Whereas ten animals from group Ila and Ilb after 4, 8 and 12 weeks of the study. Results obtained showed that serum and liver arylesterase and paraoxonase activities were significantly decreased in infected mice after 8, 12 weeks as compared to controls. The activities of these enzymes were partially restored in infected animals received zinc. Four bands of arylesterase isoenzymes were detected in Dolyacrelamide gel electrophoresis of control liver mice with or without zinc supplementation, infected liver mice after 4, 8 weeks and all infected liver mice in groups received zinc. The intensity Of arylesterase isoenzyme bands in infected liver mice decreased gradually during the period of the experiment. The fast migrated arylesterase isoenzyme disappeared in the infected mice after 12 weeks. These findings suggested that granuloma or inflammatory cells induced by schistosoma eggs might produce reactive oxygen intermediates which may be responsible for the reduction of these enzymatic activities in infected mice with S. mansoni. The reduction in arylesterse and paraoxonase activities in mice infected with s. mansoni was ameliorated with zinc administration and improved liver function