Cadmium Chloride-induced Toxicity Research Articles

Ameliorative role of Tetrapleura tetraptera (Schum. & Thonn.) taub in cadmium chloride-induced oxidative stress in Drosophila melanogaster using in vivo and computational approaches

BackgroundCadmium (Cd) is a naturally occurring transition metal associated with oxidative stress in living organisms. Whereas Tetrapleura tetraptera (Tt), an ethnomedicinal plant is said to possess high antioxidant activity and used to treat various human diseases locally. Therefore, the study aimed to investigate the biological activity of the ethanolic pod extract of T. tetraptera in cadmium chloride-induced toxicity in Drosophila melanogaster. MethodsSix groups of adults (1–3 days old) D. melanogaster as shown: Control, Tt 2.5 mg/10 g diet, Tt 5 mg/10 g diet, CdCl2, CdCl2+ Tt 2.5 mg/10 diet and CdCl2+Tt 5 mg/10 g diet were exposed via diet for 7 days consisting of 50 flies per vial and 5 replicate per group. Thereafter, we evaluated markers for free radical generation, antioxidant, non-antioxidant activities, and emergence rates of the flies. The active compounds of Tt extract were molecularly docked against glutathione-S-transferase II. ResultsThe results indicated that CdCl2 significantly induced oxidative stress by increasing the levels of lipid peroxidation (LPO), hydrogen peroxide (H2O2), nitric oxide (NO) and decreasing the activity of GST without an effect on total thiol (T-SH) and non-protein thiols (NP-SHs) levels. However, co-treatment with T. tetraptera (2.5 mg/10 g diet) significantly decreased levels of LPO, H2O2, but increased GST activity. Also, co-treatment with T. tetraptera (5 mg/10 g diet) increased NPSH and T-SH levels by 18.6 % and 35.8 %. Furthermore, Co-treatment (5 mg/10 g diet) increased the rate of offspring emergence. ConclusionT. tetraptera ameliorated cadmium chloride-induced oxidative stress in Drosophila melanogaster and increased offspring hatching rate. T. tetraptera may therefore serve as a good regimen for the treatment of oxidative stress-related diseases induced by cadmium.

Ameliorative activities of Moringa oleifera ethanolic leaf extract on Cadmium chloride-induced toxicity in the kidney of adult Wistar rats: A microscopic assessment

Ameliorative activities of Moringa oleifera ethanolic leaf extract on Cadmium chloride-induced toxicity in the kidney of adult Wistar rats: A microscopic assessment

Protective effects of silymarin on testis histopathology, oxidative stress indicators, antioxidant defence enzymes and serum testosterone in cadmium-treated mice.

Cadmium is known as an oxidative stress-inducing factor. Silymarin extracted from Silybum marianum is regarded as a potent antioxidant. The present study investigated the preventing effects of silymarin on cadmium chloride-induced toxicity in terms of testis histopathology and serum testosterone level as well as oxidative stress indicators in mice. In addition, the activities of antioxidant defence enzymes was evaluated. Adult male mice were divided into four groups (n=6 in each group): (a) control; (b) cadmium chloride; (c) silymarin + cadmium chloride and (d) Silymarin. In this study, cadmium chloride significantly decreased the diameter and wall thickness of the seminiferous tubule, diameter of the spermatogonia nucleus and serum testosterone levels compared to the control group. Furthermore, in mice treated with this pollutant, a significant increase in malondialdehyde was observed while ferric reducing antioxidant power level, and the activity of catalase, superoxide dismutase and glutathione peroxidase were significantly reduced in the testis. In the silymarin + cadmium chloride group, silymarin could significantly reverse the toxic effects of cadmium chloride. The findings of this study showed that silymarin, as a potent antioxidant, can compensate the adverse effects of cadmium chloride on testis histopathology, testosterone level, oxidative stress indicators and antioxidant defence enzymes in mice.

Effect of Methanol Leaf Extract of Vitex Doniana on Cadmium Chloride-Induced Toxicity in Kidney and Liver Tissues of Male Wistar Rats

Effect of Methanol Leaf Extract of Vitex Doniana on Cadmium Chloride-Induced Toxicity in Kidney and Liver Tissues of Male Wistar Rats

Betulinic acid protects mice from cadmium chloride-induced toxicity by inhibiting cadmium-induced apoptosis in kidney and liver

Cadmium exposure is closely associated with a variety of diseases including cancers and the accumulation of cadmium has been long recognized as a public health problem. It is therefore of high importance to find methods to reduce cadmium accumulation in the human body. Herein, we report that administration of betulinic acid (BA) protects mice from cadmium chloride (CdCl2)-induced toxicity by inhibiting cadmium-induced apoptosis in both kidney and liver. Mice were given oral doses of 3 mg/kg, 10 mg/kg and 30 mg/kg of BA daily for ten consecutive days, and were injected with one dose of 1 mg/kg CdCl2 after one hour of BA administration every day. The levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and blood urea nitrogen (BUN) were assessed by ELISA. Residual cadmium was determined by atomic absorption analysis. Protein expression was evaluated by western blotting. Pretreatment with BA significantly reduced residual cadmium levels in the liver, kidney and testis, increased the cadmium output in urine, and reduced tissue damage induced by CdCl2. Moreover, BA prevented body weight loss by CdCl2 in a dose dependent manner. Furthermore, BA treatment increased the expression levels of B-cell lymphoma 2 (Bcl-2), decreased Bcl-2-associated X (Bax), and inhibited the levels of active caspase-3. Importantly, BA within a dose of 30 mg/kg did not induce any signs of toxicity, and protected mice from the toxicity induced by CdCl2 in a dose-dependent manner. Our findings suggest that BA inhibits CdCl2 induced apoptosis in the kidney and liver, and BA may be an effective agent for the prevention and treatment of cadmium-induced diseases in humans.

Cadmium Chloride Induces DNA Damage and Apoptosis of Human Liver Carcinoma Cells via Oxidative Stress.

Cadmium is a heavy metal that has been shown to cause its toxicity in humans and animals. Many documented studies have shown that cadmium produces various genotoxic effects such as DNA damage and chromosomal aberrations. Ailments such as bone disease, renal damage, and several forms of cancer are attributed to overexposure to cadmium. Although there have been numerous studies examining the effects of cadmium in animal models and a few case studies involving communities where cadmium contamination has occurred, its molecular mechanisms of action are not fully elucidated. In this research, we hypothesized that oxidative stress plays a key role in cadmium chloride-induced toxicity, DNA damage, and apoptosis of human liver carcinoma (HepG2) cells. To test our hypothesis, cell viability was determined by MTT assay. Lipid hydroperoxide content stress was estimated by lipid peroxidation assay. Genotoxic damage was tested by the means of alkaline single cell gel electrophoresis (Comet) assay. Cell apoptosis was measured by flow cytometry assessment (Annexin-V/PI assay). The result of MTT assay indicated that cadmium chloride induces toxicity to HepG2 cells in a concentration-dependent manner, showing a 48 hr-LD50 of 3.6 µg/mL. Data generated from lipid peroxidation assay resulted in a significant (p < 0.05) increase of hydroperoxide production, specifically at the highest concentration tested. Data obtained from the Comet assay indicated that cadmium chloride causes DNA damage in HepG2 cells in a concentration-dependent manner. A strong concentration-response relationship (p < 0.05) was recorded between annexin V positive cells and cadmium chloride exposure. In summary, these in vitro studies provide clear evidence that cadmium chloride induces oxidative stress, DNA damage, and programmed cell death in human liver carcinoma (HepG2) cells.