Antioxidant enzymes activity and lipid peroxidation in liver and kidney of rats exposed to cadmium and ethanol.

The oxidative status of liver and kidney of rats co-exposed to cadmium (50 mg Cd/l in drinking water) and ethanol (5 g EtOH/kg body weight/24 h, intragastrically) for 12 weeks was studied. The activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT) as well as the concentration of malondialdehyde (MDA), as an indicator of lipid peroxidation, were measured in homogenates of the liver and kidney. Concentrations of zinc (Zn), copper (Cu), iron (Fe) and Cd in the serum or blood, and their content in the liver and kidney as well as EtOH concentration in the whole blood were assayed. Daily Cd intake in the Cd and Cd+EtOH groups was similar and ranged from 2.39 to 4.88 mg/kg body weight/24 h and from 2.64 to 4.14 mg/kg body weight/24 h, respectively. After the administration of EtOH alone, the activity of SOD increased in the kidney and decreased in the liver, whereas the activity of CAT decreased in both these organs, and MDA concentration increased in the liver and was unchanged in the kidney. The exposure to 50 mg Cd/l led to a decrease in the activities of SOD in the liver and CAT in the liver and kidney, and an increase in the kidney activity of SOD and MDA concentration in both these organs. In the rats co-exposed to Cd and EtOH, the kidney activity of SOD and the liver concentration of MDA were lower, whereas the kidney activity of CAT was higher compared to the Cd group. The concentration of Fe in the serum and its content in the liver of rats treated with EtOH increased, whereas the concentrations of Zn and Cu in the serum and the content of Zn, Cu and Fe in the kidney and that of Zn and Cu in the liver were unchanged. In the liver and kidney of rats treated with Cd alone, the content of Fe was decreased and that of Zn and Cu was enhanced. After EtOH administration to Cd-exposed rats, a decrease in Cu serum concentration and its liver content and an increase in Fe concentration in the serum and its content in the liver and kidney, compared to the group exposed to Cd alone, were noted. Moreover, EtOH decreased the blood Cd concentration and its accumulation in the liver and kidney of these animals. EtOH alone decreased Cd content in the liver and increased in the kidney, however the whole content of Cd in these organs was unchanged compared with control. The results of this study indicate that despite the ability of Cd and EtOH to induce the oxidative stress the effect in the liver and kidney is not intensified at simultaneous exposure to both substances. The changes in the studied indicators of oxidative stress (SOD, CAT and MDA) observed in the kidney and especially in the liver of the rats co-exposed to Cd and EtOH may result from an independent effect of Cd and/or EtOH and also from their interaction. The interactive effect may involve, among others, changes in Cd accumulation and content of Zn, Cu and Fe in these organs and their concentration in serum. Since the rats treated with Cd and Cd+EtOH had reduced drinking fluids intake that might result in dehydratation, the effect of the both xenobiotics on the oxidative status of the body may be not solely due to Cd and/or EtOH, but also the modyfing influence of accompanying alterations such as reduced water intake and dehydratation. The results of the study allow us to hypothesize that Cd-exposed alcohol misusers are not at enhanced risk of liver and kidney damage due to lipid peroxidation.

A preliminary study of the submandibular gland of the rat after one-year cadmium intoxication. Part I. Cadmium concentration.

The aim of the present study was to establish to what degree a one-year exposure of rat females to 5, 50 and 100 mg Cd/l affects the weight of the submandibular glands and their cadmium levels. We observed a decrease in the weight of the submandibular glands in the rat females from Groups I, II and III, compared to the control rats. We also found an increase in cadmium levels in the submandibular glands in Groups I, II and III, in comparison to the control. The highest cadmium concentration was noted in the submandibular glands in Group III, which was accompanied by the greatest weight reduction, the correlation being negative. The present experiment indicates that one-year administration of cadmium to rat females at a dose of 5, 50 and 100 mg Cd/l leads to a cadmium dose-dependent decrease in the weight of the submandibular glands.

Cadmium turnover and changes of zinc and copper body status of rats continuously exposed to cadmium and ethanol.

The effects of continuous exposure to cadmium (Cd) and ethanol on Cd turnover and zinc (Zn) and copper (Cu) body status of male Wistar rats were studied. The animals received an aqueous solution of 10% (w/v) ethanol and/or 50 mg Cd/l as the only drinking fluid for 12 weeks. The concentrations of Zn, Cu and Cd in the serum (or blood), liver, kidneys, spleen, brain, heart, femoral muscle and femur as well as in 24-h urine and faeces specimens were assessed by atomic absorption spectrometry (AAS). Ethanol alone had no effect on Cd accumulation or excretion. By contrast, co-administration of ethanol with Cd influenced the turnover of this toxic metal. Long-term consumption of ethanol alone caused a decrease in femur Zn and liver Cu concentrations. Moreover, the urinary loss of both bioelements decreased, whereas their faecal excretion was increased. Exposure to Cd resulted in an increase in liver and kidney and in a decrease in femur and 24-h urine Zn concentrations. An increase in Cu concentration in the kidney and a decrease in the brain were also noted. Moreover, Cd increased the total pool of Zn in organs (kidneys, liver, spleen, heart and brain), but did not influence that of Cu. Zn concentration in the liver, kidney and spleen of rats co-exposed to Cd and ethanol were increased, but were decreased in the brain and femur, compared to controls. The concentrations of Cu in livers and brains of these rats were decreased, whereas those in kidney, spleen and heart were increased. The urinary excretion of the elements was decreased, whereas their faecal excretion was increased. Moreover, the total amount of Cu in organs decreased below the control value and that of Zn was in the normal range. These changes in Zn and Cu levels could be explained by different effects of both toxic substances, differences in bioelement intakes (due to reduced consumption of drinking solutions and food), and the modifying effect of ethanol on Cd turnover. Our results suggest that alcoholics may be more susceptible to Cd accumulation and its effects on body Zn and Cu.

The effect of zinc supply on cadmium-induced changes in the tibia of rats.

It has been determined that zinc supplementation (240 microg Zn/ml) during (for 12 weeks) or after (for 2 weeks) cadmium exposure (50 microg Cd/ml for 12 weeks) can prevent the accumulation and toxic action of Cd in the tibia of rats. The exposure to Cd led to disturbances in bone metabolism reflected by changes in the chemical composition of bone and decreased bone mineral density (osteomalacian changes). The Zn supply in conditions of Cd intoxication completely prevented the Cd-induced increase in percentage of water content and decrease in tibia ash weight, ash weight/dry weight, non-org. comp./org. comp., Zn content and concentration. Moreover, Zn partly protected from the decrease in Ca concentration and content, percentage of non-organic components content, Ca/wet weight, Ca/ash weight and Ca/dry weight. Zn administered after Cd exposure partly, but not completely, protected from Cd-induced decrease in percentage of non-organic components content, Ca/wet weight as well as Ca content and concentration. This protective effect on bone was most evident when Zn was administered during Cd exposure. But Zn, independently of the manner of its administration, did not prevent Cd accumulation in the tibia. Our results suggest that Zn supply in conditions of simultaneous exposure can prevent Cd-induced bone loss to some extent, and used after Cd treatment can give therapeutic benefits.

Effect of short-term ethanol administration on cadmium retention and bioelement metabolism in rats continuously exposed to cadmium.

The present study was performed to assess the effect of short-term ethanol administration on cadmium retention and accumulation as well as on bioelement metabolism (zinc, copper, calcium, and magnesium) in rats exposed to an aqueous solution of cadmium chloride for 8 weeks. Intoxication with cadmium led to accumulation of this toxic metal, particularly in the liver and kidney, which was linked to metallothionein synthesis as well as to a disturbance in the metabolism of zinc, copper, and calcium. These effects were dependent on the level of exposure. The administration of ethanol in the final phase of cadmium treatment increased cadmium retention and accumulation in the body with simultaneous elevation in liver and kidney metallothionein concentration. Ethanol alone or with cadmium caused or intensified the cadmium-induced changes in metabolism of zinc and copper. Calcium metabolism disturbed by cadmium was not influenced by ethanol. Neither agents had any effect on magnesium metabolism. We conclude that even short-term ethanol consumption in conditions of exposure to cadmium can increase this heavy metal body burden and lead to more serious disturbances in metabolism of important elements such as zinc and copper. Cadmium- and ethanol-induced changes in the homeostasis of these microelements are probably connected with the ability of both xenobiotics to cause metallothionein induction.

Influence of ethanol on the activity of glycosidases in rats exposed to cadmium (Cd2+).

Inhibition by ethanol of the activities of lysosomal exoglycosidases in stomach, small intestine, liver and brain of rats exposed to cadmium (Cd2+) was determined. Out of the glycosidases tested the most distinct effect of Cd2+ and ethanol administered to the rats in vivo was observed in the small intestinal mucosa in a decreasing order: N-acetyl-beta-hexosaminidase, beta-galactosidase and alpha-fucosidase.