# Protective role of astaxanthin against bisphenol A induced biochemical and histopathological alterations in rat kidneys

**Authors:** Burcu Gültekin, Seda Çetinkaya Karabekir, İlknur Çınar Ayan, Hasan Basri Savaş, Serpil Kalkan

PMC · DOI: 10.22038/ijbms.2025.88356.19081 · Iranian Journal of Basic Medical Sciences · 2025-01-01

## TL;DR

This study shows that astaxanthin can protect rat kidneys from damage caused by bisphenol A, a common toxin linked to kidney disease.

## Contribution

The novel contribution is demonstrating astaxanthin's protective effect against BPA-induced kidney damage in a rat model.

## Key findings

- Astaxanthin reversed BPA-induced inhibition of PON1 and ARE enzyme levels and reduced elevated urea levels.
- BPA caused kidney tissue damage including vacuolization and collagen increase, which were improved by astaxanthin treatment.
- Astaxanthin partially inhibited BPA-induced apoptosis in kidney tissue.

## Abstract

This study investigates the ability of astaxanthin (ASTX), a powerful anti-oxidant, to protect kidney tissue from oxidative and cellular damage resulting from bisphenol A (BPA) toxicity, a widespread global toxin associated with chronic kidney disease.

We used 32 male Wistar Albino rats, 16 weeks old, and weighing 250–300 g. The rats were randomly divided into four groups: Control, Sham, BPA, and BPA+ASTX. Following the experiment, serum samples were assessed for Paraoxonase 1 (PON1), Arylesterase (ARE), urea, and creatinine levels. Changes in kidney tissue induced by BPA were examined using histopathological methods. Also, the levels of apoptosis and collagen content were evaluated.

ASTX treatment reversed the BPA-induced inhibition of PON1 and ARE levels, restoring them to control levels, and reduced the BPA-induced increase in urea levels. Creatinine levels showed no significant differences across the groups. BPA exposure in kidney tissue caused vacuolization, congestion, tubular dilatation, desquamation, infiltration, and increased collagen around glomeruli and blood vessels. However, ASTX treatment significantly improved these pathological findings. While BPA induced apoptosis as indicated by Bax and Bcl-2 analysis, ASTX treatment partially inhibited this process.

These findings indicate that ASTX may protect against BPA-induced renal injury. However, the study’s limitations include the use of a single dose and a focus solely on kidney tissue. Additionally, the lack of dose-response data and evaluations of other organs or long-term effects are significant drawbacks. Future research should explore multiple doses and longer observation periods for a better understanding of ASTX’s protective efficacy.

## Linked entities

- **Proteins:** PON1 (paraoxonase 1), are (Arylesterase), BAX (BCL2 associated X, apoptosis regulator), BCL2 (BCL2 apoptosis regulator)
- **Chemicals:** astaxanthin (PubChem CID 5281224), bisphenol A (PubChem CID 6623), urea (PubChem CID 1176), creatinine (PubChem CID 588)
- **Diseases:** chronic kidney disease (MONDO:0005300)

## Full-text entities

- **Genes:** Bax (BCL2 associated X, apoptosis regulator) [NCBI Gene 24887], Pon1 (paraoxonase 1) [NCBI Gene 84024], Bcl2 (BCL2, apoptosis regulator) [NCBI Gene 24224] {aka Bcl-2}
- **Diseases:** chronic kidney disease (MESH:D051436), renal injury (MESH:D007674), toxicity (MESH:D064420)
- **Chemicals:** ASTX (MESH:C005948), urea (MESH:D014508), Creatinine (MESH:D003404), BPA (MESH:C006780)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12829686/full.md

## References

58 references — full list in the complete paper: https://tomesphere.com/paper/PMC12829686/full.md

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Source: https://tomesphere.com/paper/PMC12829686