Effects of Melatonin and Epiphyseal Proteins on Fluoride-Induced Adverse Changes in Antioxidant Status of Heart, Liver, and Kidney of Rats

Abstract

Several experimental and clinical reports indicated the oxidative stress-mediated adverse changes in vital organs of human and animal in fluoride (F) toxicity. Therefore, the present study was undertaken to evaluate the therapeutic effect of buffalo (Bubalus bubalis) epiphyseal (pineal) proteins (BEP) and melatonin (MEL) against F-induced oxidative stress in heart, liver, and kidney of experimental adult female rats. To accomplish this experimental objective, twenty-four adult female Wistar rats (123–143 g body weights) were divided into four groups, namely, control, F, F + BEP, and F + MEL and were administered sodium fluoride (NaF, 150 ppm elemental F in drinking water), MEL (10 mg/kg BW, i.p.), and BEP (100 µg/kg BW, i.p.) for 28 days. There were significantly (P < 0.05) high levels of lipid peroxidation and catalase and low levels of reduced glutathione, superoxide dismutase, glutathione reductase, and glutathione peroxidase in cardiac, hepatic, and renal tissues of F-treated rats. Administration of BEP and MEL in F-treated rats, however, significantly (P < 0.05) attenuated these adverse changes in all the target components of antioxidant defense system of cardiac, hepatic, and renal tissues. The present data suggest that F can induce oxidative stress in liver, heart, and kidney of female rats which may be a mechanism in F toxicity and these adverse effects can be ameliorated by buffalo (Bubalus bubalis) epiphyseal proteins and melatonin by upregulation of antioxidant defense system of heart, liver, and kidney of rats.

Fluoride-induced iron overload contributes to hepatic oxidative damage in mouse and the protective role of Grape seed proanthocyanidin extract

“…Our results are consistent with a previous report showing an elevated liver MDA level in mice experimentally intoxicated with fluoride (Nabavi et al, 2013). Similarly, Bharti et al (2014) demonstrated that the levels of GSH-Px, T-AOC, and SOD were decreased in the livers of rats experimentally exposed to fluoride. Altogether, these findings suggest that fluoride alters intracellular redox homeostasis and induces oxidative stress by inhibiting the activity of antioxidant enzymes.…”

Melatonin promotes hepatic differentiation of human dental pulp stem cells: clinical implications for the prevention of liver fibrosis

“…Melatonin (N-acetyl-5-methoxytryptamine), a naturally occurring neurohormone derived from amino acid tryptophan, is produced in a circadian manner by the pineal gland [15]. Exogenous melatonin has been demonstrated to possess a number of anti-inflammatory and antioxidant effects in vivo and in vitro [16][17][18][19][20][21][22][23]. Recently, we demonstrated that melatonin exerted cytoprotective and antiinflammatory effect in an oxidative stress-stimulated chondrocyte model as well as rabbit osteoarthritis model via SIRT1 pathway [24].…”

The state of oxidative-antioxidant homeostasis under the influence of subtoxic doses of sodium fluoride

“…In subsequent experiments of Bharti V. and others, a number of biochemical parameters were studied reflecting the state of the antioxidant system and the redox processes represented by the enzyme system [10]. In addition to the enzyme activity (in organs and tissues) of catalase, peroxidase, ceruloplasmin, lactate and malate dehydrogenases, cholinesterase, glucose-6-phosphate dehydrogenase, alanine and aspartic aminotransferases, alkaline phosphatase (Table 5), studied in a subacute experiment.…”