Microscopic and ultrastructural insights into the protective role of melatonin against tartrazine-induced hepatotoxicity.

Tartrazine, a coal tar-derived azo color, is utilized in food, drinks, cosmetics, and pharmaceuticals. Its azo group catabolizes in the gut, poisoning the liver. This study investigated the efficacy of melatonin, an endogenous antioxidant from the pineal gland against hepatotoxicity in tartrazine-intoxicated rats. Thirty-two adult male wistar albino rats were allocated into four groups: control group, melatonin group (10 mg/kg), tartrazine-treated group (7.5 mg/kg), and tartrazine + melatonin-treated group (7.5 mg/kg tartrazine + 10 mg/kg melatonin). Doses were taken daily for 4 weeks. Melatonin's influence on hepatotoxicity was assessed by monitoring liver enzyme activity, antioxidant state, apoptotic and inflammatory markers, DNA fragmentation, histological and ultrastructural changes. Rats exposed to tartrazine exhibited elevated liver enzymes, oxidant-antioxidant imbalance, and elevated hepatic inflammatory markers (TNF-α, IL-6). Tartrazine also damaged DNA and induced histological and ultrastructural alterations in liver tissue, as shown by the comet assay. Alpha-fetoprotein (AFP) and proliferating cell nuclear antigen (PCNA) were strongly expressed in immunohistochemistry. In rats, melatonin significantly reduced all tartrazine effects. Conversely, melatonin treatment significantly alleviated all aforementioned effects induced by tartrazine in rats by decreasing liver enzymes, elevating antioxidant enzymes, and reducing hepatic inflammatory markers. Enhanced histological assessment and the ultrastructure of the liver was detected following melatonin use. The use of melatonin may safeguard against tartrazine-induced hepatic DNA damage. In conclusion, the current findings indicate that tartrazine administration has detrimental health effects and deleterious impacts on liver function and structure. Melatonin mitigated tartrazine-induced liver damage via antioxidant, anti-inflammatory, and anti-apoptotic pathways.