Methyl 3-O-methyl gallate (M3OMG), a naturally-occurring compound of limited distribution, can be readily synthesized from methyl gallate. In the present study, the protective effect of M3OMG of synthetic origin on fluoride-induced cardiotoxicity and oxidative stress in cardiac tissues of rats was evaluated. After intraperitonial administration of M3OMG (10 and 20 mg/kg bw), or the positive control (ascorbic acid at 10 mg/kg bw), for seven consecutive days, rats were intoxicated by fluoride (F) with sodium fluoride (NaF) at 600 ppm in their drinking water for a further week. The level of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) and the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were examined in the cardiac homogenates. The results showed that F intoxication caused a significant abnormality in the levels of TBARS and GSH as well as in the activities of antioxidant enzymes in cardiac tissues. M3OMG at the dose of at 20 mg/kg bw significantly suppressed the NaF-induced enhanced level of TBARS. M3OMG also restored the NaF-induced abnormality in the activities of SOD and CAT and the level of GSH in cardiac tissues. Ascorbic acid (vitamin C) at 10 mg/kg bw also showed a comparable amelioration of the NaFinduced toxicity in the rat heart. Taking all the results together, M3OMG demonstrated a notable cardioprotective role against NaF-induced toxicity and oxidative stress in rat cardiac tissues.

PROTECTIVE EFFECT OF METHYL 3-O-METHYL GALLATE AGAINST SODIUM FLUORIDE-INDUCED OXIDATIVE STRESS IN RAT CARDIAC TISSUES

DAGLIA, MARIA;
2012-01-01

Abstract

Methyl 3-O-methyl gallate (M3OMG), a naturally-occurring compound of limited distribution, can be readily synthesized from methyl gallate. In the present study, the protective effect of M3OMG of synthetic origin on fluoride-induced cardiotoxicity and oxidative stress in cardiac tissues of rats was evaluated. After intraperitonial administration of M3OMG (10 and 20 mg/kg bw), or the positive control (ascorbic acid at 10 mg/kg bw), for seven consecutive days, rats were intoxicated by fluoride (F) with sodium fluoride (NaF) at 600 ppm in their drinking water for a further week. The level of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) and the activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were examined in the cardiac homogenates. The results showed that F intoxication caused a significant abnormality in the levels of TBARS and GSH as well as in the activities of antioxidant enzymes in cardiac tissues. M3OMG at the dose of at 20 mg/kg bw significantly suppressed the NaF-induced enhanced level of TBARS. M3OMG also restored the NaF-induced abnormality in the activities of SOD and CAT and the level of GSH in cardiac tissues. Ascorbic acid (vitamin C) at 10 mg/kg bw also showed a comparable amelioration of the NaFinduced toxicity in the rat heart. Taking all the results together, M3OMG demonstrated a notable cardioprotective role against NaF-induced toxicity and oxidative stress in rat cardiac tissues.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11571/625613
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