International Journal of Occupational Medicine and Environmental Health · 2 authors, 1 centre
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
This review of 57 studies (50 animal, 7 human) finds that vitamins E, C, A, and β-carotene reduce cadmium-induced oxidative stress and tissue damage across multiple organ systems in animal models. Human studies show associations between higher antioxidant vitamin levels and lower cadmium biomarkers, but results are inconclusive. The findings support promoting dietary antioxidant intake in populations exposed to cadmium.
**Background:** Cadmium (Cd) is a toxic heavy metal that accumulates in the environment and enters the human body primarily through diet and smoking. Chronic Cd exposure causes oxidative stress and damage to multiple organ systems, including renal, hepatic, cardiovascular, skeletal, and reproductive systems. Antioxidant vitamins (E, C, A, β-carotene) may mitigate Cd toxicity by scavenging reactive oxygen species and enhancing antioxidant defenses. This narrative review summarizes evidence from animal and human studies on the protective effects of these vitamins against Cd-induced toxicity.
**Methods:** A literature search was conducted in PubMed using keywords: cadmium and vitamin E, vitamin C, vitamin A, or β-carotene. Inclusion criteria: English language, full-text articles, published January 1, 1980–April 30, 2021, focusing on Cd exposure and antioxidant vitamin use. Of 310 articles identified, 57 original studies were included: 50 in vivo animal studies and 7 human studies.
**Key Results:** - **Vitamin E:** In animal models, vitamin E (doses 1.5–400 mg/kg) reduced oxidative stress markers (MDA, TBARS), increased antioxidant enzymes (SOD, CAT, GPx), and improved histopathology in liver, kidney, testis, and brain. It also decreased Cd accumulation, apoptosis, and improved hematological parameters. Two human studies showed negative correlations between blood Cd and serum vitamin E in smokers, but no modification of Cd-leukocyte telomere length (LTL) association. - **Vitamin C:** In animals, vitamin C (10–150 mg/kg) reduced liver enzymes (ALT, AST), improved renal function (creatinine, urea), decreased oxidative stress, and reduced Cd accumulation in tissues. Human studies showed negative associations between vitamin C intake and blood Cd in pregnant women, but supplementation (500–1000 mg/day) did not alter Cd levels in hair or blood. - **Vitamin A:** Animal studies showed vitamin A (75 mg/kg or 500 IU/kg) reduced ALT, improved histopathology in liver, kidney, testis, and lung, and increased metallothionein. Human studies found positive associations between serum retinol and bone mineral density, and between vitamin A and LTL, but no modification of Cd-LTL association. - **β-Carotene:** In rats, β-carotene (10 mg/kg or 250 IU/kg) reduced oxidative stress in liver, testis, and brain, and improved semen quality. Human studies showed negative correlations between serum β-carotene and blood Cd in smokers, and between urinary Cd and serum β-carotene in peripheral arterial disease patients.
**Clinical Implications:** The review supports a potential protective role of antioxidant vitamins against Cd toxicity, particularly in animal models. However, human evidence is limited and inconsistent. Promoting dietary intake of vitamin E (plant oils), vitamin C (fruits, vegetables), vitamin A (dairy, liver), and β-carotene (yellow/green vegetables) may be a reasonable public health strategy for populations with occupational or environmental Cd exposure. Further well-designed human studies are needed to clarify dose-response relationships and long-term benefits.