Metanil yellow suppresses contraction mediated ejection functions of heart ventricular muscle by inducing fibrillar and mitochondrial oxidative stress

Abstract

The presence of metanil yellow (MY), a synthetic azo-dye, has been scientifically proved in different food products. It is mostly used in unorganized food industries as a food colorant due to its cost-effectiveness. Humans are often exposed to MY through ingested food products, colored with MY. The toxic effects of MY have already been reported in animal models. Till date, the effects of MY on heart ventricular functions have not been reported. So, our study was aimed to evaluate the effects of MY on the functions of heart ventricular muscle in rat model in vivo. We have observed significant (P<0.05) increase in the level of malondialdehyde and content of reduced glutathione in heart ventricular muscle of MY exposed groups of rats in comparison with control rats. The enzymatic activities of cytosolic copper-zinc-superoxide dismutase, glutathione peroxidase, glutathione reductase; and mitochondrial manganese superoxide dismutase and ATPase were significantly (P<0.05) increased in exposed groups. Whereas the activities of cytosolic catalase and acetylcholinesterase; mitochondrial catalase, Krebs cycle and electron transport chain enzymes were decreased significantly (P<0.05). Furthermore, myodegeneration of heart ventricular muscle and myofibrillar mitochondria of exposed rats have been identified through prominent signs of lesions and disintegrations by scanning electron microscopic and histological studies. So, from our observations we can conclude that MY depresses the contraction mediated ejection functions of heart, probably by inducing fibrillar and mitochondrial oxidative stress in heart ventricular muscle. The results obtained through this study in rat model could be extrapolated in humans.