Protective Effect of Grape and Apple Juices against Cadmium Intoxication in the Kidney of Rats.

BACKGROUND: The objective of this study was to evaluate protective effect of grape and apple juices against toxicity induced by cadmium in the kidney of rats. METHODS: A total of 20 male-Wistar rats were distributed into four groups (n=5): Control group: animals received an intraperitoneal (i.p.) injection of 0.9% saline solution and after 15 days, 1 mL of water was administered for 15 days, via gavage; Cadmium group: animals received an intraperitoneal injection of cadmium chloride (1.2 mg/kg) and after 15 days, 1 mL of water was administered for 15 days via gavage; Cadmium+Grape Juice: animals received an i.p. injection of cadmium chloride (1.2 mg/kg), and after 15 days, 0.8 mL of grape juice was administered for 15 days, via gavage; Cadmium+Apple Juice: animals received i.p. injection of cadmium chloride (1.2 mg/kg) and after 15 days, 1.0 mL of apple juice was administered for 15 days, via gavage. RESULTS: Histopathological analysis revealed severe tubular lesion and necrosis in the group exposed to cadmium, while animals exposed to grape or apple juices showed a significant reduction of tissue injury. 8-OHdG immunoexpression, DNA damage, cytochrome C and catalase gene expressions and Toll like signaling pathway (TLR2, and pIKKα/ß) decreased in animals treated with grape juice when compared to cadmium group. CONCLUSION: Taken together, we conclude that grape and apple juices had a protective effect by means of antioxidant, antigenotoxic actions and for promoting tissue regeneration in the kidney of rats following cadmium intoxication.

Neuro- and nephrotoxicity of subchronic cadmium chloride exposure and the potential chemoprotective effects of selenium nanoparticles.

Cadmium (Cd) exposure leads to production of reactive oxygen species (ROS), which are associated with Cd-induced neurotoxicity and nephrotoxicity. Selenium nanoparticles (Se-NPs) have high bioavailability and antioxidant activities so it attracted wide spread attention. The present study examined the possible ameliorative effect of Se-NPs with diameters of 3-5 nm and 10-20 nm against cadmium chloride (CdCl2)-induced neuro- and nephrotoxicity in rats. Rats were treated with Se-NPs (0 or 0.5 mg/kg BW, s.c.) one hour prior to the CdCl2 (0 or 5 mg/kg BW, p.o.). Pretreatment with Se-NPs significantly decreased CdCl2-induced elevation of serum kidney and brain damage biomarkers; lipid peroxidation; the percent of DNA fragmentation and nearly normalized the activity of acetylcholinesterase (AchE) and significantly increased the activity and expression of antioxidant biomarkers in the RNA and protein levels. Se-NPs also attenuated CdCl2-induced upregulation of kidney and brain pro-apoptotic B-cell CLL/lymphoma 2 associated X (Bax) RNA and protein levels with preventing the increased body burden of Cd and the altered Fe and Cu homeostasis. Histopathological analysis confirmed the biochemical and molecular outcomes. Our data stated that Se-NPs appear to be effective in ameliorating the adverse neurological and nephrotoxic effects induced by CdCl2 partially through the scavenging of free radicals, metal ion chelation, averting apoptosis and altering the cell-protective pathways. The results indicated that Se-NPs could potentially included as an additive to Cd-based industries to control Cd-induced brain and renal injury.

Heavy metals toxicity: effect of cadmium ions on amyloid beta protein 1-42. Possible implications for Alzheimer's disease.

Cadmium (Cd) is an environmental contaminant, highly toxic to humans. This biologically non-essential element accumulates in the body, especially in the kidney, liver, lung and brain and can induce several toxic effects, depending on the concentration and the exposure time. Cd has been linked to Alzheimer's disease (AD) as a probable risk factor, as it shows higher concentrations in brain tissues of AD patients than in healthy people, its implication in the formation of neurofibrillary tangles and in the aggregation process of amyloid beta peptides (AßPs). AßPs seem to have toxic properties, particularly in their aggregated state; insoluble AßP forms, such as small and large aggregates, protofibrils and fibrils, appear to be implicated in the pathogenesis of AD. In our study, we have evaluated the effect of Cd, at different concentrations, both on the AßP1-42 ion channel incorporated in a planar lipid membrane made up of phosphatidylcholine containing 30 % cholesterol and on the secondary structure of AßP1-42 in aqueous environment. Cadmium is able to interact with the AßP1-42 peptide by acting on the channel incorporated into the membrane as well as on the peptide in solution, both decreasing AßP1-42 channel frequency and in solution forming large and amorphous aggregates prone to precipitate. These experimental observations suggesting a toxic role for Cd strengthen the hypothesis that Cd may interact directly with AßPs and may be a risk factor in AD.

Effect of wheat bran and flaxseed on cadmium effects and retention in rats.

Dietary fiber can affect cadmium (Cd) absorption and toxicity, but the effect appears to depend on the type of dietary fiber. The aim of the present study was to compare the effect of dietary sources containing distinct amounts of soluble and insoluble fiber on Cd absorption, accumulation and toxicity in growing rats. The absorption of essential macrominerals (Ca, P and Mg) was also evaluated. Animals received a nutritionally balanced diet with cellulose (cel - control), wheat bran or flaxseed as the fiber source with 0 or 50 mg Cd kg(-1) diet, during 30 days. Cd exposure reduced body weight gain, feed efficiency ratio, epididymal fat relative weight and liver relative weight, and increased plasma alanine aminotransferase activity in all fiber groups. The apparent Cd absorption was similar among Cd-groups, but the flax-Cd group had a higher hepatic and renal Cd concentration. Cd decreased the absorption of Ca and P, and increased Mg absorption in the wheat bran and flaxseed groups, but not in the cel group. Although the different fiber sources investigated had no effect on Cd toxicity, the major soluble fiber source, flaxseed, increased Cd retention. Thus, caution should be taken in the intake of flaxseed by Cd-exposed populations.

Effects of cadmium ions on the initial stage of translation and the cell death in mouse liver.

OBJECTIVE: To evaluate in vivo and in vitro effects of cadmium ions on the activities of mice liver tRNA(Leu)and leucyl-tRNA synthetase and on the type of liver cells death. MATERIAL AND METHODS: White laboratory mice were intoxicated by intraperitoneal injection of cadmium chloride solution (1.6 mg cadmium ions/1 kg of body weigh). Total tRNAs were isolated by adding ethanol and isopropanol into the phenol-deproteinized supernatant of mouse liver homogenate. Post-mitochondrial fraction of the liver cells was used as a source of leucyl-tRNA synthetase. Acceptor activity of tRNA(Leu)and activity of leucyl-tRNA synthetase were measured in tRNA aminoacylation reaction with [14C]-labeled leucine as a substrate. An apoptotic cell death was assessed by the TUNEL assay using in situ cell death detection kit. DNA degradation was verified by electrophoresis. RESULTS: It was determined that 2-24 hours after intoxication with sublethal dose of cadmium ions the acceptor activity of mice liver tRNA(Leu)was decreased by 43-73% as compared to control. At the same time intervals, the activity of leucyl-tRNA synthetase was reduced about 20-30%. Experiments in vitro revealed that 10-20 microM concentrations of cadmium ions suppressed the activities of mice liver tRNA(Leu)and leucyl-tRNA synthetase by 40-98%. No significant difference was observed between the number of TUNEL positive apoptotic liver cells in the control mice and 24 hours after intoxication with cadmium chloride. Electrophoresis revealed extensive degradation of nuclear DNA. CONCLUSIONS: Cadmium ions significantly reduce activities of tRNA(Leu)and leucyl-tRNA synthetase in vivo and in vitro. There is no significant difference between the number of apoptotic cells in the control liver specimens and in those after 24 hours of intoxication with cadmium chloride. In latter specimens DNA electrophoresis revealed as extensive degradation of DNA, which is characteristic to the cell necrosis.

The effect of cadmium on the immune behaviour of guinea pigs with experimental ascariasis.

The subchronic effect of cadmium on selected immunological parameters was studied in guinea pigs with experimental ascariasis. Cadmium chloride given orally for 28 days caused a considerable suppression of T- and B-cells in the lymphoid organs of intoxicated animals, of the metabolic activity of their peritoneal macrophages and a moderate decline in the level of complement CH50 and AH50 from day 1 to day 28 of the experiment, in comparison with the initial value. After a subsequent infection of the subchronically intoxicated guinea pigs the values for both the cell populations and the macrophage metabolic activity remained considerably suppressed, compared with infected control animals. The phagocytic and metabolic activity of macrophages as well as the CH50 and AH50 level, however, increased conspicuously for a short time after application of heavy metal and after infection but it did not reach the level of the infected group. The level of specific circulating antibodies was not affected by intoxication. Compared with the controls, the mean intensity of infection with Ascaris larvae migrating in the lungs of intoxicated animals increased by 20%. The results have established the negative effect of cadmium on the immunological parameters of the cellular immunity and humoral immunity studied and the impairment of the organism's response to the antigenic stimulus after an A. suum infection.