Antioxidant and ACE enhancing potential of Pankajakasthuri in fluoride toxicity: Anin vitrostudy on mammalian lungs

Abstract

Fluoride toxicity occurs due to high concentrations of fluoride in water sources or anthropogenic causes. The aim of the present study was to investigate the effects of an Ayurvedic drug--Pankajakasthuri (PK)--in relation to fluoride-induced toxicity in mammalian lungs. The results indicated that sodium fluoride increased lipid peroxidation and decreased enzymatic and non-enzymatic antioxidants in a concentration-dependent manner in lungs. The antioxidant potential of the lungs was suppressed maximally at 10 ppm fluoride concentration and PK at all three dose levels (i.e., 100, 200 and 300 µl) decreased fluoride induced lipid peroxidation (p < 0.05) and increased the levels of total ascorbic acid, superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase and FRAP values significantly (p < 0.05) in a dose-dependent manner. When PK was examined for its effects on angiotensin-converting enzyme (ACE) activity, in fluoride-induced toxicity, the ACE activity was found to increase (p < 0.0001) in lung homogenates with all three doses. This study indicates that PK, an Ayurvedic drug, improves mammalian lung function by increasing antioxidant potential and ACE activity under the conditions of fluoride toxicity.

Effect of Pomegranate Seed Oil against Hepatotoxicity- Induced by Sodium Fluoride in Adult Female Rats (Part II).

“…The results also showed changes in biomarkers of oxidative stress as evidenced by a decrease of reduced glutathione and an increase in peroxynitrite concentrations. Fluoride is known to reduce intracellular GSH levels and inhibit various enzymes that require GSH as a cofactor (66). Besides, (14) reported that, a reduction in GSH content and in the activity of antioxidant enzymes in the liver of rats exposed to SF indicating an impaired function of the hepatic antioxidant defense system (67) associated to an increase of LPO (56).…”

The Effects of Melatonin on Brain Injury in Acute Organophosphate Toxicity

“…The activity of ACE localized in erythrocyte membranes is a significant indicator of OP poisoning severity (13). In previous studies (chronic and subchronic exposure) in rats and humans, acute OP poisoning erythrocyte ACE activity was not significantly different than levels in healthy controls (Tinoco & Halperine, 1998;Öğüt et al, 2011). On the contrary, in a rat study of subchronic OP exposure, erythrocyte ACE activity and TBARS levels were found to be significantly lower in the toxicity group compared to healthy controls (Lukaszewicz-Hussain & Moniuszko-Jakoniuk, 2005).…”

Role Of Pomegranate Seed Oil (PSO) Against Hepatotoxicity Induced By Sodium Fluoride In Adult Female Rats (Part II)

“…The results also showed changes in biomarkers of oxidative stress as evidenced by a decrease of reduced glutathione and an increase in peroxynitrite concentrations. Fluoride is known to reduce intracellular GSH levels and inhibit various enzymes that require GSH as a cofactor (67).Besides, (1) reported that, a reduction in GSH content and in the activity of antioxidant enzymes in the liver of rats exposed to SF indicating an impaired function of the hepatic antioxidant defense system (27) associated to an increase of LPO (72). This deterioration overlaps with the elimination of H 2 O 2 and LPO products and causes their accumulation in the cells leading to the damage of cell membranes and may affect the activity of these enzymes which constituting the cell anti-oxidative system (37).…”