2, 3-Dimethylsuccinic acid and fulvic acid attenuate lead-induced oxidative misbalance in brain tissues of Nile tilapia Oreochromis niloticus

Abstract

Lead has long been known as neurotoxic and immunotoxic heavy metal in human and animals including fish, whereas, 2, 3-dimethylsuccinic acid (DMSA) and fulvic acid (FA) are well-known biological chelators. The present investigation was carried out to assess the potential chelating and antioxidant effects of dietary supplementation with DMSA and FA against lead acetate (Pb)-induced oxidative stress in Nile tilapia, O. niloticus. One-hundred and eighty apparently healthy O. niloticus fish (30 ± 2.5 g) were allocated into six equal groups. The first group was fed on basal diet and served as control, while the second group was fed on DMSA-supplemented basal diets at levels of 30 mg/kg diet; the third group was fed on FA-supplemented basal diet at level of 0.3 mg/kg diet; the forth, fifths, and sixth groups were exposed to 14.4 mg Pb /L water (1/10 LC50) and feed on basal diet only, basal diet supplemented with DMSA (0.3 mg/kg diet), or basal diet supplemented with FA (0.3 mg/kg diet), respectively. Antioxidant and lipid peroxidative status, activity of glucose 6-phosphate dehydrogenase (G6PD), and lactate dehydrogenase (LDH) as well as the histopathologic findings were evaluated in brain tissues, while the Pb residues were evaluated in liver, muscles, and brain tissues. The results of the present study showed that DMSA and FA decreased malondialdehyde (MDA) and Pb residue in tissues of Pb-exposed fish and improved the histologic picture and brain contents of glutathione (GSH), glutathione-s-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), G6PD, LDH, and total antioxidant capacity (TAC). It could be concluded that DMSA and FA supplementation exhibited potential neuroprotective effect against Pb-induced oxidative brain damages in O. niloticus through improvement of antioxidant status of the brain tissue.

Keywords: 2, 3-Dimethylsuccinic acid; Fulvic acid; Glucose-6-phosphate dehydrogenase; Lead acetate; Lipid peroxidation; Oreochromis niloticus; Tissue residue.