Evaluation of ascorbic acid as an intervention of metal toxicity in dogs in Kabwe district

Non-essential metals and metalloids are known to induce oxidative stress in exposed organisms, often leading to cellular damage and systemic toxicity. While chelation therapy remains the primary treatment for metal toxicity, its application is limited by side effects. L-ascorbic acid (L-AA), a widely available antioxidant, has emerged as a promising nutritional intervention for mitigating metal-induced oxidative stress. Dogs, whose blood lead levels (BLLs) closely mirror those of humans, have been utilized as sentinel species in environmental toxicology studies. This study aimed to evaluate the therapeutic potential of L-AA in dogs residing in Kabwe, Zambia, a former mining town where remediation of heavy metal contamination is ongoing. The reported BLLs in Kabwe dogs ranged from 0.43 µg/dL to 123.5 µg/dL. A total of 22 dogs (10 females and 12 males) received oral L-AA supplementation daily for 14 days. Blood samples were collected on Day 1 of L-AA administration and Day 14 to assess biochemical and toxicological changes. Post-treatment analysis revealed statistically significant reductions in plasma malondialdehyde, cortisol, blood urea nitrogen, and creatinine levels, as determined by Student's t-test and Wilcoxon signed-rank test. Additionally, δ-aminolaevulinic acid dehydratase activity was significantly elevated, indicating improved oxidative status. These findings support the efficacy of L-AA in attenuating oxidative stress associated with metal and metalloid exposure, even in the absence of exposure cessation. Interestingly, Pb levels declined predominantly in dogs younger than 24 months. Furthermore, reductions in Zn and Cu commonly linked to L-AA administration were observed exclusively in male dogs, suggesting a sex-specific response.