Investigation of the protective effects of polydatin and grape seed extracts on blood, liver, kidney, brain and testis tissues, oxidant-antioxidant parameters and histopathological changes in rats exposed to cadmium

Awareness against toxic factors such as cadmium requires more advance researches and protection in a sustainable manner for these factors. In this regard, it is important to use antioxidant phytochemical substances effectively and safely. The current study aimed to investigate the protective role of polydatin (PD) and grape seed extracts (GSE) against the oxidative effects of cadmium chlorine application in the blood, liver, kidney, brain and testis tissues of rats. Atotal of 49 adult Wistar albino male rats was used in our study. Rats were divided into seven equal groups: Control group (Normal saline), Cd group (5 mg/kg CdCI2), PD group (120 mg/kg PD), GSE group (120 mg/kg GSE), Cd+PD group (5 mg/kg CdCI2 + 120 mg/kg PD), Cd+ GSE group (5 mg/kg CdCI2 + 120 mg GSE), and Cd+PD+ GSE group (5 mg/kg CdCI2+120 mg/kg PD + 120 mg/kg GSE). Cd, PD, and GSE were prepared in saline and administered by oral gavages for 4 weeks. At the end of the experimental period, all rats were decapitated and their blood, liver, kidney, brain and testis tissue samples were examined histopathologically. Cadmium accumulation, total oxidant and antioxidant status, malondialdehiyde levels and antioxidant potentials were also measured in blood and tissues. According to ICP-OES data, when compared the control group to other treatments, Cd accumulation was observed in all tissues studied except for the brain tissue. Cd levels in brain tissue could not be determined since it was under ICP-OES measurement limits. PD and GSE inhibited the Cd accumulation in erythrocytes and tissues at varying levels. Histopathological examination of liver, kidney, brain and testes showed extensive degenerative changes in Cd treated group. Mild degenerative changes were seen in the CD+PD, CD+GSE and CD+PD+GSE groups. PD and GSE alone reduced the histopathological changes in the same tissues. The TOS data indicated that PD and GSE did not suppress Cd induced oxidative stress in blood plasma. Liver TOS level in Cd group increased significantly compared to the control. In addition, the phytochemicals used in the study also reduced TOS levels in liver. TOS values from kidney, brain and testis tissues suggest that PD and GSE did not show a strong antioxidant effect in these tissues. MDA levels in blood plasma and liver tissues raised significantly in Cd treated rats compared to controls. PD, GSE and their combinations significantly decreased the MDA levels in blood plasma and liver tissue. However, PD and GSE showed no significant positive effect against Cd exposure in kidney, brain and testis MDA levels. Compared to the cadmium administration, PD, GSE and their combinations significantly increased AOP levels in plasma, liver, kidney and brain tissues. In the testis, AOP levels improved in PD and GSE groups. On the other hand, compared to Cd group there was no positive effect on AOP levels observed in the groups that antioxidant phytochemicals administered with cadmium. Consequently, Cd exposure in rats showed oxidative damage, particularly in blood and liver. On the other hand, kidney, brain and testis tissue did not exhibit very strong oxidative stress because of Cd. Although the protective effects of PD and GSE were detected at different levels in different tissues, the protective effects of PD have been shown to be more effective than GSE. Our results suggested that although the initiation of histopathological changes were present in all tissues, the initiating factor was not the oxidative stress in the tissues studied except for the liver and blood.