Malondialdehyde [MDA] and reduced glutathione [GSH] levels in maternal and umbilical serum in women with mild and moderate pre-eclampsia

Increased oxidative stress and lipid peroxidation associated with impairment of the anti-oxidant systems has been found to be involved in the pathogenesis of many diseases. Evaluation of such a role in pregnancy-related pathophysiological conditions seems to be important in this respect. The present study was designed to evaluate the possibility of the involvement of lipid peroxidation and the consequent impairment of anti-oxidant activities in pair-matched maternal and umbilical cord serum in pre-eclamptic pregnant women. Fifteen healthy normotensive women, six women with mild pre-eclampsia, and six with moderate pre-eclampsia, were involved in the study in Abu-Ghraib Hospital. Serum levels of malondialdehyde [MDA] and reduced glutathione [GSH] levels in * peripheral blood before and immediately after delivery and in the umbilical cord. Before delivery, maternal serum levels of MDA and GSH were higher and lower, respectively in both cases of pre-eclampsia when compared with normal pregnant. In umbilical cord serum, the appearance of MDA were lower than the corresponding maternal values, while serum levels of GSH is higher. No differences were observed between umbilical cord serum and maternal serum concerning MDA and GSH levels after delivery. This study suggests that, lipid peroxidation is involved in the pathogenesis of maternal pre-eclampsia. The presence of protective mechanism against lipid peroxides in placental system is indicated by increased level of GSH in umbilical cord serum

Effect of silymarin on renal levels of free calcium and trace elements in gentamicin-induced nephrotoxicity in rats

Aminoglycosides antibiotics are nephrotoxic, with most of the damage confined to the proximal convoluted tubules. But the mechanism for cellular toxicity is not clear; whether inhibition of mitochondrial respiration and calcium transport or lipid per oxidation were claimed to be the causes of irreversible cell damage. Silymarin as a natural remedy for diseases of the liver necessitates the evaluation of the efficiency of this compound and its possible mode of action on the ameliorating the injury induced by xenobiotics or drugs on tissues other than the liver. The aim of this study was designed to investigate the possible effect of silymarin on amelioration of renal injury induced by gentamicin and the consequences of nephrotoxicity by measuring changes in zinc, cupper and calcium homeostasis, which may play a role in gentamicin-induced nephrotoxicity. Kidney tissue homogenate from normal controls, gentamicin-treated, and silymarin 250 mg/hg pre-treated before the induction of renal toxicity with gentamicin in Rattus norvigicus rats were obtained, and processed for the estimation of free calcium levels, trace elements, [zinc and cupper] levels using atomic absorption spectrophotometry. [AAS]. Analysis of data revealed significant decrease in the levels of free calcium, copper and in copper over zinc ratio, while there is an increase in the level of zinc in kidney tissue homogenate in the animals pre-treated with silymarin when compared to gentamicin-treated animals. These findings suggest that, silymarin is effective in ameliorating the consequences of renal cell injury evoked by gentamicin as evidenced by decreasing the levels of free calcium and copper with the reduction in cupper/zinc ratio, and elevation in the level of zinc in kidney tissue homogenate

effect of different doses of silymarin on gentamicin-induced kidney damage in rats

Many in vivo and in vitro studies performed mainly in liver have been shown silymarin to be a potent anti-oxidant, and one of the most potent scavengers of hydroxyl radicals. Therefore, it is plausible to expect that it may produce these effects against oxidalive stress consequences induced by gentamicin in the kidney. Evaluation of the protective effect of different doses of silymarin given orally in protecting rats against gentamicin-induced nephrotoxicity. Groups of rats [6 rats each] were pre-treated for 7 days with 250, 500, and l000 mg/kg silymarin and vehicle orally before induction of renal toxicity with gentamicin, and another 6 rats were utilized as controls. The parameters of oxidative stress, malondialdehyde [MDA], and glutathione [GSH] were measured in the serum and kidney tissue homogenate, in addition to serum levels of urea and creatinine. Histopathological examination of stained tissue sections from the kidney was performed; in addition to silymarin level in the kidney tissue homogenate was evaluated using HPLC method. Analysis of data revealed significant amelioration of oxidative stress, experimentally induced in the kidney through lowering MDA and elevation of GSH levels, both in serum and tissue homogenate, associated with significant reduction of serum levels of urea and creatinine, and with positive histological evidences for the protective effect of silymarin which is found to be related to the increase in its renal tissue availability when the oral dose was increased. These findings suggest that, silymarin is effective in preventing gentamicin-induced renal toxicity, which makes it a good candidate for clinical use in this respect

Dose-dependent protective effects of silymarin against ccu-induced liver damage in rats

Silymarin, the dried extract of the ripe seeds of Silybum marianum is found to be a powerful protective agent against xenobiotics-induced tissue injury in many organs, including liver. However, the dose-dependent relationship of this effect and tissue availability is not fully explored. So, this project was designed to evaluate the relationship between dose, tissue availability and tissue protection of silymarin against ccu-induced hepatic toxicity in rats. The tissue protective effects of silymarin were studied through the pre-treatment of rats with various doses [250, 500, and l000 mg/kg] orally twice daily before the induction of hepatotoxicity of ccl4. Malondialdehyde [MDA] and glutathione [GSH] were evaluated in the serum and tissue homogenate. The activities of different enzymes, which are considered as indicators of organ toxicity like alanine amino transaminase [ALT] and aspartate aminotransaminase [AST] were assessed. Histopathological examination of stained tissue sections from the liver were done to evaluate the protective effect at the microscopical levels. In addition, silymarin level in liver tissue homogenate -was evaluated using HPLC method. The data obtained indicated that, a significant amelioration of oxidative stress experimentally induced in the liver of rats was produced by silymarin, as evidenced by lowering MDA contents and elevation of GSH levels both in the tissues and serum compared with controls. Serum activities of ALT and AST were normalized. Additionally, histologically evident damage in the liver had improved In addition, increasing silymarin dose after oral administration resulted in increased tissue availability of many constituents. There is a dose-dependent relationship in the hepatoprotective effect of silymarin against ccU-induced hepatotoxicity in rats