Almost all heavy metals are serious toxicants as carcinogens. However, due to their chemical and physiological properties, heavy metals are useful in industrial areas including alloy, smelting and production of commercial products. Such applications increase the opportunity for heavy metal exposure. Waste from industrial processes is also a major source of environmental contamination and accumulation in the human body. Arsenic, cadmium, chromium, and nickel are classified as group 1 carcinogens by the International Agency for Research on Cancer, and are utilized commercially. In this review, we used molecular pathway analysis to understand the toxicity and carcinogenic mechanisms of these metals. Our analyzed data showed that above-mentioned metallic substances induce oxidative stress, DNA damage, and cell death processes, resulting in increase the risk of cancer and cancer-related diseases. Thus, we might think phytochelatin molecules and antioxidative phytochemical substances are helpful for prevention of heavy metal-induced cancer.

An Overview of Carcinogenic Heavy Metal: Molecular Toxicity Mechanism and Prevention.

Cadmium (Cd) is a non-essential transition metal which is introduced into the biosphere by various anthropogenic activities. Environmental pollution with Cd poses a major health risk and Cd toxicity has been extensively researched over the past decades. This review aims at changing the perspective by discussing protection mechanisms available to counteract a Cd insult. Antioxidants, induction of antioxidant enzymes, and complexation of Cd to glutathione (GSH) and metallothionein (MT) are the most potent protective measures to cope with Cd-induced oxidative stress. Furthermore, protection mechanisms include prevention of endoplasmic reticulum (ER) stress, mitophagy and metabolic stress, as well as expression of chaperones. Pre-exposure to Cd itself, or co-exposure to other metals or trace elements can improve viability under Cd exposure and cells have means to reduce Cd uptake and improve Cd removal. Finally, environmental factors have negative or positive effects on Cd toxicity. Most protection mechanisms aim at preventing cellular damage. However, this might not be possible without trade-offs like an increased risk of carcinogenesis.

https://www.mdpi.com/1422-0067/17/1/139/pdf

Cadmium Protection Strategies--A Hidden Trade-Off?

Cadmium chloride-induced testicular toxicity in male wistar rats; prophylactic effect of quercetin, and assessment of testicular recovery following cadmium chloride withdrawal.

Quercetin exerts preventive, ameliorative and prophylactic effects on cadmium chloride - induced oxidative stress in the uterus and ovaries of female Wistar rats

Summary
Exposure to cadmium (Cd) reduces sperm quality and induces oxidative stress in the testis. Rutin is an effective antioxidant flavonoid. We studied the effect of ethanol (EtOH, 5 g/kg b.wt.) intake on Cd (50 mg/kg b.wt.)-induced testicular toxicity with or without RUT pre-treatment (25, 50, 100 mg/kg b.wt.) in rats. At the end of the 15-day oral treatment, co-treatment with EtOH decreased the activities of glutathione (GSH), GSH-peroxidase and superoxide dismutase resulting to slight increase in the testicular MDA level compared to Cd-treated rats. The Cd+EtOH animals had higher levels of abnormal spermatozoa, decreased epididymal sperm number and serum testosterone levels (p < .05) compared to the Cd-treated animals. Rutin co-administration protected against the EtOH effects in a dose-dependent manner, with the Cd+EtOH+50 mg/kg RUT- and Cd+EtOH+100 mg/kg RUT-treated animals having higher GSH and GSH-Px activities beyond the control values (p < .05). In a supplementary study, animals treated daily with RUT alone (25, 50, 100 mg/kg b.wt.) for 15 days dose-dependently increased testicular GSH-peroxidase and GSH activities by 9.38%, 31.25%, 56.25% and 7.14%, 32.14%, 60.71%, respectively, compared to control values. Therefore, RUT induces GSH and GSH-Px activities to protect against Cd+EtOH-induced testis oxidative stress in rats.

Rutin, an antioxidant flavonoid, induces glutathione and glutathione peroxidase activities to protect against ethanol effects in cadmium-induced oxidative stress in the testis of adult rats.

The present study was conducted to compare and evaluate the potential benefits of three different antioxidants in reversing cadmium (Cd)-induced reproductive toxicity in adult male rats. Rats (n = 5) weighing 180 ± 20 gm were divided into five groups (control, Cd, Cd + sulforaphane, Cd + vitamin E, and Cd + plant extract). Treated groups received CdCl2 (0.2 mg/kg), sulforaphane (25 µg/rat), vitamin E (75 mg/kg), and plant extract (100 mg/kg) for 15 days. Blood samples and testicular tissues were obtained for estimation of testosterone, Zn, and Cd concentration and daily sperm production/efficiency of sperm production. Cadmium exposure caused a significant decrease in final body weight (p < 0.0001). The plasma concentrations of Cd were significantly increased and Zn concentration decreased (p < 0.0001) in the Cd group as compared to the control group. The testicular concentrations of Cd were significantly increased and Zn concentration decreased (p < 0.0001) in the Cd group as compared to the contr...

https://www.tandfonline.com/doi/pdf/10.3109/19396368.2013.843039

Mehreen Khan

Papers

Comparative analysis of antioxidants against cadmium induced reproductive toxicity in adult male rats