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

**Authors:** Nelly Banda, Mahongo Selwa, Rio Doya, Nyein Chan Soe, Andrew Kataba, John Yabe, Golden Zyambo, Kaampwe Muzandu, Yared Beyene Yohannes, Yoshinori Ikenaka, Mayumi Ishizuka, Shouta MM Nakayama

PMC · DOI: 10.1016/j.vas.2025.100519 · 2025-10-09

## TL;DR

This study shows that vitamin C (L-ascorbic acid) can reduce oxidative stress and metal levels in dogs exposed to heavy metals in Kabwe, Zambia.

## Contribution

The study demonstrates the effectiveness of L-ascorbic acid in reducing metal toxicity in dogs, with age- and sex-specific responses.

## Key findings

- L-ascorbic acid significantly reduced oxidative stress biomarkers in dogs.
- Lead levels decreased mainly in dogs under 24 months of age.
- Zinc and copper reductions were observed only in male dogs after treatment.

## Abstract

•Oxidative stress biomarkers were reduced in dogs after administration of L-ascorbic acid.•The reduction of BLL occurred mostly in younger dogs under 24 months of age.•The reduction of Pb, AS, and Cd occurs in both males and females.•The reduction of essential metals, Cu and Zn, occurs in male dogs but not in females post-treatment with L-ascorbic acid.

Oxidative stress biomarkers were reduced in dogs after administration of L-ascorbic acid.

The reduction of BLL occurred mostly in younger dogs under 24 months of age.

The reduction of Pb, AS, and Cd occurs in both males and females.

The reduction of essential metals, Cu and Zn, occurs in male dogs but not in females post-treatment with L-ascorbic acid.

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.

Image, graphical abstract

## Linked entities

- **Chemicals:** L-ascorbic acid (PubChem CID 54670067), lead (PubChem CID 5352425), arsenic (PubChem CID 5359596), cadmium (PubChem CID 23973), copper (PubChem CID 23978), zinc (PubChem CID 23994)
- **Species:** Canis lupus familiaris (taxon 9615)

## Full-text entities

- **Diseases:** toxicity (MESH:D064420), metal toxicity (MESH:D000075322)
- **Chemicals:** L-AA (MESH:D001205), metal (MESH:D008670), creatinine (MESH:D003404), Cu (MESH:D003300), Pb (MESH:D007854), heavy metal (MESH:D019216), metalloid (MESH:D058955), cortisol (MESH:D006854), malondialdehyde (MESH:D008315), Zn (MESH:D015032)
- **Species:** Canis lupus familiaris (dog, subspecies) [taxon 9615], Homo sapiens (human, species) [taxon 9606]

## Figures

13 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12554065/full.md

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Source: https://tomesphere.com/paper/PMC12554065