The present study highlights fluoride -induced toxicity and the protective role of ascorbic acid in the liver and ovary of freshwater fish, Heteropneustis fossilis. The fish specimens were exposed to different concentrations (35 mg F/L and 70 mg F/L) of fluoride. Parameters related to oxidative stress were studied at the end of the experiment. The biomarkers selected for the study were thiobarbituric acid reactive substances for assessing the extent of lipid peroxidation (LPO) and antioxidant defense system such as reduced glutathione (GSH), superoxide dismutase (SOD) catalase (CAT) glutathione peroxidase (GPx), and glutathione S-transferase (GST) activities. The fluoride exposure significantly elevated the level of LPO, CAT, SOD, and GST in the tissues of treated group as well as modulated the activities of GSH and level of GPx after exposure as compared to the control. A significant decrease in GPx activity was found in these tissues suggesting that fluoride exposure increases the level of free radical, as well as CAT activity. Pre- and post treatment with ascorbic acid decreased the LPO, SOD, CAT, GST level, and increased GSH, GPx levels in the liver and ovary.
-
-
Mitigating effects of some antidotes on fluoride and arsenic induced free radical toxicity in mice ovary
The effects of oral administration of sodium fluoride (NaF) and/or arsenic trioxide (As(2)O(3)) (5 mg and 0.5 mg/kg body weight, respectively) for 30 days were investigated on free radical induced toxicity in the mouse ovary. The reversibility of the induced effects after withdrawal of NaF+As(2)O(3) treatment and by administration of
-
Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants
The objective of the present communication is to address the issues concerning reversal of fluoride induced cell injury and disease (i.e. fluorosis) through the elimination of fluoride and consumption of a diet containing essential nutrients and antioxidants. Humans afflicted with fluorosis, as a result of consuming fluoride contaminated water or
-
Toxic effects of fluoride and chlorpyrifos on antioxidant parameters in rats: protective effects of vitamins C and E
In continuing our studies on the effects of fluoride (F) on the toxicity of pesticides, we investigated the interaction of 1 ppm and 10 ppm F in the drinking water of rats orally administered 1 and 10 mg chlorpyriphos/kg bw/day, alone and in combination for 28 days. Changes in antioxidant
-
Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain
CONTEXT: Quercetin is a well known aglycone flavonoid that is widely found in different food sources. OBJECTIVE: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated. MATERIALS AND METHODS: Wistar rats were divided into five treatment groups and then subjected to daily
-
Protective role of gallic acid on sodium fluoride induced oxidative stress in rat brain
Gallic acid is known as a potent antioxidant active compound of the edible and medicinal plant Peltiphyllum peltatum. The main objective of this study was to evaluate the neuroprotective effects of gallic acid against sodium fluoride induced oxidative stress in rat brain. Gallic acid (10 and 20 mg/kg) and vitamin C
Related Studies :
-
-
-
Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
-
Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
-
Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
-
Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
-
Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
Related FAN Content :
-