What question did this study set out to answer?

To assess the protective effects of astaxanthin against bisphenol A-induced testicular toxicity in rats.

February 21, 2026Biomolecules and Biomedicine0 citationsOpen Access

Astaxanthin attenuates bisphenol A–induced testicular toxicity in Wistar rats by reducing apoptosis and fibrosis via Bax/Bcl-2 balance and collagen gene expression

HCHalime Tuba Canbaz MSMehmet Enes Sözen IAIlknur Cinar Ayan

Key Points

To assess the protective effects of astaxanthin against bisphenol A-induced testicular toxicity in rats.
Four experimental groups of Wistar rats (Control, Sham, BPA, BPA+AST) were established.
Evaluated biochemical markers of oxidative stress and inflammation.
Histopathological analyses of testicular tissues were performed.
Immunofluorescence and RT-qPCR assessed Bax/Bcl-2 levels and collagen gene expression.
BPA group showed increased total oxidant status and CRP levels with decreased Johnsen scores.
AST treatment improved Johnsen scores and tubule diameters compared to the BPA group.
AST normalized Bax expression but did not significantly affect Bcl-2 levels.
Collagen gene expressions were elevated in the BPA group and reduced by AST treatment.

Abstract

Bisphenol A (BPA), a synthetic compound widely used in plastic manufacturing, has been shown to cause testicular damage and disrupt spermatogenesis. This study aimed to investigate the potential protective effects of astaxanthin (AST) against BPA-induced testicular injury. Four experimental groups of Wistar Albino rats were established (n=8 per group): Control, Sham, BPA, and BPA+AST. At the conclusion of the study, serum samples were analyzed for total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI) OSI=TOS/TAC, and CRP. Histopathological evaluations included measurements of tubule diameter, Johnsen scoring, and Masson's trichrome staining. The expression levels of anti-B-cell lymphoma 2 (Bcl-2) and anti-Bcl-2-associated X protein (Bax) were assessed using immunofluorescence (IF) staining and RT-qPCR in testicular tissues. Additionally, tissue collagen (COL1A1, COL3A1) expressions were quantified via RT-qPCR. Results indicated significant increases in TOS, OSI, and CRP levels in the BPA group (p<0.001, p<0.001, and p=0.042, respectively), while TAC levels remained unchanged (p=0.119). AST administration did not significantly alter these biochemical parameters. Histopathological analysis revealed decreased Johnsen scores and tubule diameters in the BPA group; however, these metrics improved in the BPA+AST group. IF analysis confirmed that AST restored the pro-apoptotic Bax/Bcl-2 imbalance induced by BPA (p<0.001), although RT-qPCR results indicated that AST normalized only Bax expression (p<0.001) while Bcl-2 levels remained unchanged (p=0.487). Moreover, COL1A1 and COL3A1 were significantly upregulated in the BPA group (p<0.001 for both), and Masson's trichrome staining corroborated the presence of fibrosis in this group. AST treatment mitigated these fibrotic changes, as evidenced by reductions in gene expression (p=0.001 for COL1A1 and p=0.005 for COL3A1) and improvements in Masson's trichrome staining. In conclusion, this study suggests that AST may confer a protective effect against BPA-induced testicular damage by reducing apoptosis and fibrosis; however, changes in oxidative stress markers did not achieve statistical significance. Furthermore, AST may enhance spermatogenesis.

问 AI

Bookmark

View Full Paper