Tartrazine, A Food Coloring Agent Exacerbate Streptozotocin-Induced Testicular and Epididymal Toxicity: A Study in Diabetic Rat Models

Abstract

The present study investigated the probable effect of a food coloring agent, tartrazine on male reproductive health in streptozotocin-induced diabetic rats. Healthy male rats were divided into three groups(n =8 per group) wherein rats in group I served as controls and rats in group II, and III were treated as diabetic rats which were injected with streptozotocin (STZ). In addition, rats in groups III wereorally administered with tartrazine (TTZ: 500 mg/Kg BW) over a period of 60 days. In diabetic rats, a significant reduction in the relative weights of reproductive organs, testicular daily sperm count, epididymal sperm count, sperm motility, sperm viability and sperm membrane integrity, circulatory levels of serum testosterone and the activity levels of testicular 3β- and 17β-hydroxysteroid dehydrogenases were observed over untreated rats. A significant increase in the circulatory levels of follicle stimulating hormone and luteinizing hormone in diabetic rats were observed over controls. Significant elevation in the lipid peroxidation levels and hydrogen peroxide content accompanied by a significant reduction in the activity levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in the testis of diabetic rats were observed over untreated rats. RT-qPCR analysis revealed that the expression levels of steroidogenic acute regulatory protein (StAR) mRNA was observed in the testis of diabetic rats. The testicular architecture was disorganized in STZ-induced diabetic rats. Interestingly, oral administration of TTZ further deteriorated the selected reproductive variables in STZ-induced diabetic rats as compared to STZ alone treated rats. Furthermore, the fertility efficacy of STZ plus TTZ administered rats was deteriorated as compared to STZ alone treated rats. In silico analysis also indicated that TTZ can able to occupy the same ligand binding pocket and compete with cholesterol, an endogenous ligand for StAR protein thereby interferes with testosterone biosynthesis. From the results, it can be concluded that the administration of TTZ accelerate the adverse on testicular functions in STZ-induced diabetic rat models.