The effect of L-carnitine on oxidative stress responses of experimental contrast-induced nephropathy in rats.

This study was conducted to investigate the prophylactic effects of carnitine against contrast-induced nephropathy (CIN) and its relation to oxidant/antioxidant status in kidney, liver, heart, spleen and lung tissues in a CIN rat model. Twenty-eight adult male Wistar rats were divided into 4 groups, the control, contrast media (CM), carnitine and contrast media+carnitine (CM+carnitine) groups. Animals were placed in individual metabolism cages, and on the 2nd day, rats were deprived of water for 24 hr. On the 3rd day, contrast media were administered to groups CM and CM+carnitine. L-carnitine was administered on days 2, 3 and 4. Histopathological changes were evaluated in the right kidney after euthanization. Superoxide dismutase (SOD) and catalase (CAT) activities and glutathione (GSH) and malondialdehyde (MDA) levels were measured in renal, liver, heart, spleen and lung tissues. The SOD activities in the renal (P<0.05), liver (P<0.001) and spleen (P<0.05) tissues were increased in the carnitine group. The CAT activities in the spleen tissue were decreased (P<0.01) only in the CM group. Renal (P<0.05), liver (P<0.001), spleen (P<0.001) and lung tissue (P<0.01) GSH levels were found to be higher in the carnitine group. In renal, liver and lung tissues, the MDA levels increased in the CM group (P<0.001). The histopathological findings showed that L-carnitine may have a preventative effect in alleviating the negative effects of CIN. Similar to this, L-carnitine may play a major role in the stability of the antioxidant status in the kidney, liver, spleen and lung of the CIN rat model.

Effects of melatonin and dexpanthenol on antioxidant parameters when combined with estrogen treatment in ovariectomized rats.

The purpose of the study was to assess whether it is possible to reduce the oxidative damage using antioxidant agents combined with hormone replacement therapy after menopause. In this prospective experimental study, 50 mature female Wistar albino rats weighing 270-310 g were used. Rats were divided into the following six groups: (1) Ovx group (n = 7): the animals underwent bilateral ovariectomy. No drug was administered following bilateral ovariectomy. (2) Ovx + E 2 group (n = 7): bilateral ovariectomy + 17ß-estradiol (100 µg/kg/day); (3) Ovx + E 2 + MT5 group (n = 7): bilateral ovariectomy + 17ß-estradiol (100 µg/kg/day) + melatonin (5 mg/kg/day); (4) Ovx + E 2 + MT20 group (n = 7): bilateral ovariectomy + 17ß-estradiol (100 µg/kg/day) + melatonin (20 mg/kg/day); (5) Ovx + E 2 + Dxp250 group (n = 7): bilateral ovariectomy + 17ß-estradiol (100 µg/kg/day) + dexpanthenol (250 mg/kg/day); (6) Ovx + E 2 + Dxp500 group (n = 7): bilateral ovariectomy + 17ß-estradiol (100 µg/kg/day) + dexpanthenol (500 mg/kg/day), and the activity of these antioxidative enzymes and oxidative stress products were measured. Enzymatic activity levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase(GSH-Px), and glutathione reductase and levels of free radicals (malondialdehyde (MDA) and nitric oxide) were both analyzed. We observed an increase in the level of GSH activity, but no significant differences in levels of CAT, SOD, and GSH-Px enzymatic activity and in levels of free radical MDA following 17ß-estradiol or additional antioxidant treatment (melatonin or dexpanthenol). Despite the present study indicating that the addition of melatonin and dexpanthenol into the hormone replacement therapy regimen may contribute to the antioxidant effect of estrogen, the existence of limited data in this field indicates that further studies are warranted.