Cisplatin (CDDP), one of the most active cytotoxic agents against cancer, has adverse side effects, such as nephrotoxicity and hepatotoxicity. The present study was designed to investigate the potential protective effect of pomegranate seed extract (PSE) against oxidative stress caused by CDDP injury of the kidneys and liver by measuring tissue biochemical and antioxidant variables and immunohistochemically testing caspase-3-positive cells. Twenty-four Sprague-Dawley rats were divided into 4 groups: control; CDDP: injected intraperitoneally with CDDP (7 mg/kg body weight, single dose); PSE: treated for 15 consecutive days by gavage with PSE (300 mg/kg per day); and PSE+CDDP: treated by gavage with PSE 15 days after a single injection of CDDP. The degree of protection against CDDP injury afforded by PSE was evaluated by determining the levels of malondialdehyde as a measure of lipid peroxidation. The levels of glutathione and activities of glutathione peroxidase, glutathione S-transferase, and superoxide dismutase were estimated from liver and kidney homogenates; the liver and kidney were also histologically examined. PSE elicited a significant protective effect toward liver and kidney by decreasing the level of lipid peroxidation; elevating the levels of glutathione S-transferase; and increasing the activities of glutathione peroxidase, glutathione S-transferase, and superoxide dismutase. These biochemical observations were supported by immunohistochemical findings and suggested that PSE significantly attenuated nephrotoxicity and hepatotoxicity by the way of its antioxidant, radical-scavenging, and antiapoptotic effects. This PSE extract could be used as a dietary supplement in patients receiving chemotherapy medications.

Aim of this study is to evaluate protective impact of Astaxanthin (AST) on rats with experimental brain injury induced with Cadmium (Cd). 32 male Wistar albino rats were divided into four groups as Control, Cadmium, Astaxanthin (AST), Cadmium (Cd)+Astaxanthin (AST). Rat brain tissues were obtained at the end of 30 th day. Malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) enzyme activities were measured in brain homogenates and histopathological examination was performed. MDA levels were improvement in cadmium administered group (p<0.01) as well as Cd+AST administered group (p<0.05) compared to control group. In addition a substantial reduction Cd+AST group was observed compared to cadmium administered group (p<0.01). GSH level shows a decrease in Cd and Cd+AST groups compared to control (p<0.05). SOD enzyme activity was found significantly lower in Cd and Cd+AST groups compared to control (p<0.01). In addition, increase of SOD in Cd+AST group compared to cadmium group was also found significant (p<0.05). Histopathological findings in the cerebral cortex and hippocampus were different between groups. In the control and AST administered groups, normal histological structure was observed in the brain, while severe lesions were seen in the Cd administered group and in the Cd+AST group only mild degenerative lesions were observed.As a result, elevated MDA level due to Cd administration was attenuated with AST administration. Decreased GSH level and SOD enzyme activity due to Cd administration was increased with AST administration. In addition, AST administration decreased histopathological lesions. Consequently, it is thought that AST may be used for protection against brain oxidative damage due to Cd.Keywords: Astaxanthin, cadmium, oxidative stress.ÖZET: Bu çalışmada, ratlarda kadmiyum (Cd), ile meydana gelen beyin hasarını önlemede astaksantinin (AST), koruyucu etkisinin değerlendirilmesi amaçlandı. 32 adet Winstar albino cinsi rat kontol, Kadmiyum (Cd), Astaksantin (AST), Kadmiyum (Cd)+Astaksantin (AST), olmak üzere dört gruba ayrıldı. 30. Günün sonunda rat beyin dokuları alındı. Beyin doku homojenatında malondialdehit (MDA), Glutatyon (GSH) seviyeleri ve süperoksitdismutaz (SOD) enzim aktivitesi ölçülerek, histopatolojik inceleme yapıldı. Beyin dokusu MDA, düzeyleri değerlendirildiğinde kontrol grubu ile kıyaslandığında Cd uygulaması yapılan grupta (p<0,01) ve yine Cd+AST uygulanan grupta artış (p<0,05) olduğu belirlendi. Cd uygulaması yapılan gruba oranla Cd+AST grubunda görülen azalmanın istatistiksel olarak önemli olduğu belirlenmişdir (p<0,01). GSH düzeyleri değerlendirildiğinde, Cd ve Cd+AST grupları, kontrol grubu ile kıyaslandığında gruplar arasında istatistiksel olarak azalışın olduğu belirlendi (p<0,05). SOD enzim aktivitesi değerlendirildiğinde ise Cd ve Cd+AST gruplarında, kontrol grubuna kıyasla görülen azalışın (p<0,01) istatistiksel olarak önemli olduğu, Cd grubuna oranla, Cd+AST uygulaması yapılan grupta SOD düzeyinde görülen artışın önemli olduğu belirlendi (p<0,05). Hi...

In this study, we investigated the effect of astaxanthin (Ast) and aluminum (Al) on the erythrocyte glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) enzymes activities in vivo and on G6PD enzyme in vitro in rats. For in vitro studies, G6PD enzyme was purified from rat erythrocyte by using 2',5'-ADP-Sepharose 4B affinity gel. The effects of Ast and Al ion were investigated on the purified enzyme. It was determined that Ast increased the enzyme activity, whereas Al inhibited the enzyme activity noncompetitively (IC values; 0.679 mM, K values 1.32 mM). For in vivo studies, the rats were divided into the groups: control (Cont.), Al, Ast, and Al + Ast. The last three groups were compared with the control group. In Al group, a significant degree of inhibition was observed in the activity of G6PD and 6PGD enzymes when compared with the control group (P < 0.05), whereas there was an increase in the activities of G6PD and 6PGD enzymes in Ast and Al + Ast groups (P < 0.05).

In this study, the effects of astaxanthin (AST) that belongs to carotenoid family and cadmium (Cd), which is an important heavy metal, on rat erythrocyte G6PD, 6PGD, GR, and TrxR enzyme activities in vivo and on rat erythrocyte 6PGD enzyme activity in vitro were studied. In in vitro studies, 6PGD enzyme was purified from rat erythrocytes with 2',5'-ADP Sepharose4B affinity chromatography. Results showed inhibition of enzyme by Cd at IC ; 346.5 μM value and increase of 6PGD enzyme activity by AST. In vivo studies showed an increase in G6PD, 6PGD, and GR enzyme activities (P ˃ 0.05) and no chance in TrxR enzyme activity by AST. Cd ion inhibited G6PD, 6PGD, and GR enzyme activities (P ˂ 0.05) and also decreased TrxR enzyme activity (P ˃ 0.05). AST + Cd group G6PD enzyme activity was statistically low compared with control group (P ˂ 0.05). 6PGD and TrxR enzyme activities decreased without statistical significance (P ˃ 0.05); however, GR enzyme activity increased statistically significantly (P ˂ 0.05).

We investigated the possible protective effects of ellagic acid on rat kidneys exposed to nicotine during the fetal period. Twenty pregnant female rats were divided randomly into four groups: control (C), nicotine (N), ellagic acid (EA) and nicotine + ellagic acid (N + EA). Nicotine and ellagic acid treatments were continued throughout the pregnancies and for 15 days after delivery. On day 15, all neonatal pups were sacrificed and their kidneys were removed for biochemical and histopathological examination. The nicotine treatment significantly decreased body weight, total glutathione (GSH), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities, and increased malondialdehyde (MDA) and nitric oxide (NO) levels in the N group compared to controls. EA treatment ameliorated decreased body weight, GSH, GSH-Px and SOD activities, and increased MDA and NO levels in group N + EA compared to group N (p < 0.05). Nicotine caused kidney damage as shown by incomplete development of glomeruli and Bowman's capsules. Nicotine also caused greater apoptosis in group N compared to group C. Ellagic acid treatment produced histological kidney structure that was closer to normal and it exerted an anti-apoptotic effect in the N + EA group compared to the N group. EA played a protective role against nicotine-induced nephrotoxicity and oxidative stress in rats owing to its antioxidant, radical scavenging and anti-apoptotic effects.