Role of endogenous vitamin E in renal ischemic preconditioning process: differences between male and female rats

Antioxidants such as alpha-tocopherol [vitamin E] and beta-carotene [vitamin A] play an important role in protective effect of repeated brief periods of ischemia, namely ischemic preconditioning [IPC]. Values of these antioxidants were investigated and compared after induction of ischemia reperfusion [IR] and kidney IPC in both male and female rats. Forty eight Wistar rats were divided randomly into six groups of 8: groups A and B [male and female controls, respectively], group C [male IR or IR cases], group D [female IR cases] and groups E and F [male and female IPC cases, respectively]. In groups C and D, ischemia was induced by clamping of left renal arteries for 45 min. In groups E and F, rats underwent four cycles of 4 min of arterial clamping and 11 min of de-clamping before final 45 min ischemia induction. Afterward, serum was collected to assess the blood urea nitrogen, creatinine and vitamins E and A values. Renal tissues were obtained for histological assessments. alpha-tocopherol levels in male and female rats showed a significant increase in IPC compared with IR group [P<0.01] and also in female IPC compared with male IPC group. beta-carotene levels had no significant variations. Histological evaluation showed that IR-induced renal injuries were less in female rats. Also, protective effects of IPC were more in female rats [P<0.01]. Renal IPC reduced damages in both male and female rats, but tissue injuries in females were decreased much more along with the increase of endogenous vitamin E

Nitric oxide is necessary for diazoxide protection against ischemic injury in skeletal muscle

Ischemia reperfusion injury [IR injury] is a common problem in clinical conditions. Researches have frequently revealed that ATP- sensitive potassium [K[ATP]] channels and nitric oxide plays a role in protection against ischemic injury in skeletal muscle. The present study aimed at evaluating the possible link between this two pathways. Sixty-eight male wistar rats, were pretreated with saline, diazoxide [K[ATP] opener; 45 mg/Kg, IP], glibenclamide [K[ATP] inhibitor; 5 mg/Kg], or L-NAME [iNOS inhibitor; 20 mg/Kg, IP] before 3 h ischemia and 2 h reperfusion. Activities of antioxidant enzymes superoxide dismutase [SOD] and catalase [CAT], and the level of malondialdehyde [MDA] and expression of iNOS were measured in muscle tissue. Tissue MDA content was significantly increased by IR [p < 0.001]. Diazoxide significantly decreased the IR-induced elevation of tissue MDA level [p < 0.05] and Glibenclamide increased MDA [p < 0.05 vs. IR group]. L-NAME inhibited the effect of diazoxide on decreasing MDA [p < 0.01 vs., diazoxide+IR group] and IR decreased the activity of SOD and CAT [p < 0.01], while pretreatment with diazoxide increased activity of SOD and CAT [p < 0.01]. Glibenclamide decreased SOD and CAT activity after IR [p < 0.05]. L-NAME pretreatment in diazoxide-treated rats abolished the effect of diazoxide on increasing the activity of SOD and CAT [p < 0.05 vs. Diaz+IR]. Expression of iNOS was increased by IR [p < 0.01 vs. Sham group]. Diazoxide significantly decreased iNOS expression after IR [p < 0.05 vs. IR]. L-NAME significantly decreased iNOS expression after IR [p < 0.01] in diazoxide-treated rats [p < 0.01 vs. Diaz+IR]