Journal of Clinical Toxicology
Open Access
ISSN: 2161-0495
+44 1478 350008
ISSN: 2161-0495
+44 1478 350008
Ganesh Chandra Jagetia
Posters-Accepted Abstracts: J Clin Toxicol
Iron is plays a very important role in the cell metabolism and it also induces oxidative stress and several diseases. Naringin’s abilitity
to inhibit the generation of various free radicals including hydroxyl, superoxide, 2, 2-diphenyl-1-picryl hydrazyl radicals and 2,
2-azino-bis-3-ethyl benzothiazoline-6-sulphonic acid was studied and naringin inhibited these radicals in a concentration dependent
manner. The isolated mouse liver mitochondria were incubated with various concentrations of naringin before 50 μM ferric chloride
treatment. The iron overloading of caused an increase in lipid peroxidation, protein oxidation, and DNA damage in the mitochondria,
and conversely, it reduced glutathione (GSH) concentration, glutathione-S-transferase (GST), glutathione peroxidase (GSHPx),
catalase and superoxide dismutase (SOD) activities. Treatment of mitochondrial fraction with naringin before iron overloading
inhibited lipid peroxidation, protein oxidation, and DNA damage. Naringin supplementation also alleviated iron-induced depletion
in the GSH concentration, GSHPx, GST, SOD and catalase activities significantly. To understand the mechanism of action of naringin,
ferric iron reduction assay was carried out, where naringin was unable to reduce ferric iron into ferrous iron indicating that it did not
exhibit prooxidant activity. Iron free coordination site assay indicated that naringin was unable to occupy all the active sites of iron
indicating that naringin did not completely chelate iron. The present study demonstrates that naringin was able to share the burden of
endogenous oxidants by inhibiting free radicals and suppressing the iron-induced depletion of all important antioxidants and it may
be good remedy to treat iron-induced oxidative stress.