Aflatoxin B1-induced toxicity, oxido-inflammatory damage, and apoptosis in male rat reproductive circuitry were abrogated by co-treating with the xanthophyll-lutein and zeaxanthin.

Abstract

Reproductive dysfunction is a recognised adverse effect of exposure to aflatoxin B₁ (AFB₁) in humans and animals. Despite the widely acknowledged health risks, exposure to AFB₁ remains unavoidable. Conversely, lutein (LUT) and zeaxanthin (ZEA) are plants' potent antioxidants and anti-inflammatory agents, exhibiting promising potential for modulating inflammatory and apoptotic signalling pathways. This study aimed to investigate the effects of co-treatment with LUT/ZEA on reproductive function in rats intoxicated with AFB₁. The study utilised male Wistar rats (n = 20 and n = 4 per cohort). The experimental groups included untreated controls, AFB₁ (75 µg/kg), LUT/ZEA (100 mg/kg), and AFB₁ combined with LUT/ZEA at two different doses (100 mg/kg and 200 mg/kg). Treatments were administered via oral gavage for 28 consecutive days. On day 29, serum samples were collected for testicular function and hormonal assays; sperm analysis was performed; and the testes, epididymis, and brain tissues were harvested for biochemical examinations. In the AFB₁-only treated rats, there was a reduction in sperm motility, viability, and count, along with an increase in abnormal sperm morphology. The AFB₁ group exhibited hormonal dysfunction and showed increased serum alkaline phosphatase (ALP), lactate dehydrogenase (LDH) levels, and decreased acid phosphatase (ACP) levels, which were associated with reduced antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione (GSH), and total thiols (TSH) in the hypothalamus, epididymis, and testes, as well as elevated oxido-inflammatory mediators xanthine oxidase (XO), nitric oxide (NO), and myeloperoxidase (MPO). Additionally, there were changes in testicular tumour suppressor markers (p53), pro-apoptotic factors Bcl-2-associated X-protein (BAX; BAX/Bcl-2 ratio), and a reduction in anti-apoptotic biomarkers B-cell lymphoma 2 (Bcl-2). Co-treatment with LUT/ZEA alleviated the toxic effects of AFB₁, leading to improved hormonal and testicular function, enhanced antioxidant activity, and decreased levels of oxido-inflammatory mediators and apoptosis. LUT/ZEA corrected AFB₁-induced testicular dysfunction through its antioxidant, anti-inflammatory, pro-apoptotic, and anti-apoptotic properties, thereby effectively preserving testicular function and preventing testicular cell death.