Effect of boric acid on some elemental levels on rat's liver and kidney tissues during mercury chloride exposure.

In this study, the effect of boric acid on the important trace elements copper (Cu), iron (Fe), zinc (Zn), manganese (Mn) and nickel (Ni) in liver and kidney tissue of rats treated with mercury chloride was investigated. Twenty-four male Wistar albino rats (weighing 200 ± 300 g) were divided into 3 groups: Control (C), Mercury chloride (HgCl2), Mercury chloride (HgCl2) + boric acid (BA). Iron and copper were decreased whereas Mn, Zn and Ni levels were increased in liver tissue in Hg administered group compared to control. Cu (p<0.01) and Mn (p<0.001) levels were increased in Hg + BA administered group compared to Hg group. Renal tissue Cu (p<0.01), Mn and Zn levels were increased whereas Ni (p<0.05) and Fe levels were decreased in Hg administered group compared to control group. Cu (p<0.001) and Zn (p<0.05) content increased in Hg + BA group compared to control group. As a result, it is thought that boric acid may have an effect on important trace element levels such as copper (Cu), iron (Fe), zinc (Zn), manganese (Mn), nickel (Ni) in case of oxidative stress caused by mercury chloride.

Effect of astaxanthin and aluminum chloride on erythrocyte G6PD and 6PGD enzyme activities in vivo and on erythrocyte G6PD in vitro in rats.

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 Al3+ ion were investigated on the purified enzyme. It was determined that Ast increased the enzyme activity, whereas Al3+ inhibited the enzyme activity noncompetitively (IC50 values; 0.679 mM, Ki 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).

Ameliorative effects of astaxanthin against copper(II) ion-induced alteration of pentose phosphate pathway and antioxidant system enzymes in rats.

Copper (Cu) is one of the toxic elements that cause environmental pollution. As a result of excessive accumulation of copper in the organism, it causes damage in various organs and tissues and hemolysis in erythrocytes. Astaxanthin (ATX) is a pigment belonging to the xanthophyll family, which is an oxygenated derivative of carotenoids. Thanks to its powerful antioxidant properties, ATX has an extraordinary potential to protect the organism against various diseases, especially cancer. The main objective of this study was to investigate the toxic effect of copper ions on the glucose 6-phosphate dehydrogenase (G6PD), 6-phospho-gluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione S-transferase (GST), and thioredoxin reductase (TrxR) enzymes and the role of astaxanthin in reducing this effect. In in vivo study, Wistar Albino male rats (n=28) were randomly divided into 4 groups: the control group, copper (Cu2+) group, astaxanthin (ATX) group, and copper + astaxanthin (Cu2++ATX) group. The results show that G6PD enzyme activity in Cu2+ group was strongly inhibited (p ˂ 0.05), while in other groups, there were no significant effects compared to the control group (p ⩾ 0.05). 6PGD enzyme activity was significantly reduced in Cu2+ group compared to that in the control group (p ˂ 0.05), and GR enzyme activity was lower in Cu2+ group compared to that in the control group (p ˂ 0.05). Similarly, when GST enzyme activity was evaluated, a strong decrease was observed in the Cu2+ group compared to that in the control group (p ˂ 0.05), while the enzyme activity in the Cu2++ATX group approached the control group (p ⩾ 0.05). When TrxR enzyme activity level was examined, a statistically significant decrease was observed in the Cu2+ and Cu2++ATX groups (p ˂ 0.05), and the enzyme activity in the ATX group was found to be close to that in the control group. When in vitro results were evaluated, it was observed that copper ions inhibited G6PD enzyme purified from rat erythrocyte tissues with IC50=1.90 µM value and Ki = 0.97 µM ± 0.082 value and the inhibition was non-competitive. From the results, it can be concluded that Cu2+ ions have an inhibitory effect on rat erythrocyte pentose phosphate pathway and antioxidant system enzymes both in vivo and in vitro, and astaxanthin reduces this effect.

Pomegranate seed extract attenuates chemotherapy-induced acute nephrotoxicity and hepatotoxicity in rats.

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.