Effect of ischemia reperfusion on rabbit VX2 cells in a hepatocellular carcinoma model

Background: We established a rabbit VX2 cell liver carcinoma model to evaluate effects of ischemia reperfusion (IR) on reactive oxygen species (ROS) development and liver cell apoptosis rates. Methods: Thirty-six rabbits were divided into a control (n=6) and a VX2 hepatocellular carcinoma (HCC) model group (n=30), which received VX2 cell suspension injections into their livers. From the 30 HCC rabbits, 6 rabbits served as control without hepatic ischemia and the rest were treated with hepatic artery and portal vein clamps for 60 minutes. At 1 hour, 1 day, 3 days and 7 days of reperfusion, 6 rabbits were sacrificed and changes of catalase (CAT) and super-oxide dismutase (SOD) activities as well as apoptosis rates, measured by TUNEL assays, were compared between tumor tissues, normal tumor surrounding hepatic tissues and controls. Results: All treated animals developed liver tumors. The CAT activity increased in both tissues 1 hour after reperfusion (P < 0.05) and dropped to low levels in the hepatocarcinoma cells at day 1 after reperfusion (P < 0.01), but increased to higher levels than the control on day 3 (P < 0.05). SOD activity decreased significantly in both tissues until day 1 after reperfusion and kept low in the hepatocarcinoma cells until day 7 (P < 0.05). The apoptosis rates after IR increased more in cancer than in normal hepatic tissues (P < 0.01). Conclusion: Injection of VX2 tumor cell suspension into rabbit liver parenchyma achieved good results for creating a liver tumor model. IR induced apoptosis of tumor tissue and normal hepatic tissues via ROS development.     

Effect of Chronic Cholesterol Loading in the Development of Acute Ischemic Renal Failure in Rats

The effect of chronic cholesterol loading and lovastatin administration in renal artery clamping acute renal failure in rats is not known. Acute renal failure was induced by 60-min left renal artery clamping immediately afer right nephrectomy. The changes in renal function after renal artery clamping in the hyperlipidemic rats were unexpected. The acute renal failure in the cholesterol-loaded groups was less severe than in the nonhyperlipidemic rats. The lovastatin administration had some favorable effect on renal function afi ter ischemia; however, this effect was not additive to the high dietary cholesterol administration. Our results seems to favor the concept that in this special form of experimental renal ischemic acute renal failure, serum cholesterol levels, elevated through diet, may have protective effects with respect to renal tubular lesions during or following the acute ischemic insult.     

Pretreatment with Oxygen Protects Rat Kidney from Cisplatin Nephrotoxicity

Cisplatin (CP) nephrotoxicity is mainly due to reactive oxygen species. Oxygen pre-exposure as a mild oxidative stress may enhance some endogenous defense mechanisms, so its effect on cisplatin-induced acute renal failure was investigated in present study. Twenty-four rats were divided into four groups. The O₂+ CP and Air + CP groups were were subjected to i.p. injection of 5 mg/kg cisplatin, and in the Air + Saline and O₂ + Saline groups, saline was injected instead of cisplatin. O₂+ CP and O₂+ Saline groups were pretreated with oxygen (3h/d for two days), and the other two groups were pretreated with room air. Cisplatin was administered 24 h after last pretreatment session. Three days after cisplatin injection, plasma samples were obtained, and parts of kidney tissue were frozen for biochemical analysis or fixed in formalin for histological assessments. Preconditioning with oxygen prior to cisplatin administration led to reduced tubular necrosis and luminal cast formation and improvement of renal function, as was evidenced by significant reduction in plasma creatinine and urea levels. Oxygen pretreatment also significantly reversed cisplatin-induced reduction in renal catalase activity and glutathione level. It could be concluded that oxygen pretreatment could have a delayed protective effect against cisplatin nephrotoxicity, and that increased renal catalase activity may be involved in this protective effect of hyperoxia.     

Red cell antioxidant enzymes and prognostic indexes in patients with burns

Red cell superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) were measured in 66 burned patients (57 men, 9 women, age 16–78 years). BSAB varied from 15 to 93% and ABSI from 3 to 14 points. In the first week after injury the activity of SOD was significantly decreased as compared with the activity of the enzymes in the control group and was also below the reference values. Later the activity of SOD increased up to the normal range. The activity of CAT followed a similar pattern but the differences were not significant. No significant changes in red cell GPX were found during the monitored period. We did not find any significant association between the antioxidant enzyme activities and the markers of burns severity. On the other side there was a significant indirect association between the change of SOD activity (calculated as a difference between the first week values after the injury and the activities measured later) and BSAB.     

Imbalance in the antioxidant defense system as a possible cause of decreased compensatory and adaptive reserves in youths with mitral valve prolapse

An imbalance in the first line of the antioxidant defence and hyperactivity of the glutathione-dependent system were revealed in 137 youths with mitral valve prolapse. Increased activities of superoxide dismutase and glutathione reductase (by 6 and 1.82–2.10 times, respectively) can serve as an additional diagnostic criterion of decreased compensatory reserves in patients with mitral valve prolapse. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 143, No. 5, pp. 519–521, May, 2007     

Assessment of oxidative stress induced by gold nanorods following intra-tracheal instillation in rats

Gold nanorods (GNRs) are used for their wide variety of applications in various industries. There is a little availability of data related to toxicity and ecological implications of these GNRs. The study evaluated the oxidative stress induction following intra-tracheal instillation of 1 and 5?mg/kg b.w. doses of 10 and 25?nm GNRs by estimating various oxidative stress markers including lipid peroxidation (malondialdehyde; MDA), glutathione (GSH), superoxide dismutase (SOD), catalase and total antioxidant capacity (TAC) after 1?day, 1?week, 1?month, and 3?months post exposure periods. The results have shown increased MDA levels and decreased GSH levels following 1?day and 1?week post exposure periods, indicating induction of oxidative stress. Also, the SOD, catalase and TAC levels were significantly decreased following exposure of both 10 and 25?nm GNRs after 1?day and 1?week after exposures, indicating the inhibition of antioxidant defense mechanisms. Moreover, the 10?nm GNRs at 5?mg/kg dose displayed greater changes in all the estimated parameters, representing dose and size based induction of oxidative stress by GNRs. In contrast, a little change was observed during 1?month and 3?months post exposure periods, may be due to recovery. Finally, the GNRs induced dose-size-dependent oxidative stress induction by various oxidative stress markers following intra-tracheal instillation in rats.