Abstract
The effects of fipronil and fluoride co-exposure were investigated on antioxidant status of buffalo calves. A total of 24 healthy male buffalo calves divided into 4 groups were treated for 98 consecutive days. Group I, receiving no treatment, served as the control. Animals of groups II and III were orally administered with fipronil at the dosage of 0.5 mg/kg/day and sodium fluoride (NaF) at the dosage of 6.67 mg/kg/day, respectively, for 98 days. Group IV was coadministered with fipronil and NaF at the same dosages as groups II and III. Administration of fipronil alone produced significant elevation in lipid peroxidation (LPO) and decrease in the levels of nonenzymatic antioxidant glutathione (GSH). However, it did not produce any significant effect on the activities of enzymatic antioxidants including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). NaF exposure led to enhanced oxidative stress as shown by significant increase in the LPO and SOD activities while GPx and CAT activities and GSH levels were significantly decreased. Co-exposure to fipronil and NaF showed additive effects on LPO, GPx activity, and GSH levels.
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Free radical-induced nephrotoxicity following repeated oral exposure to chlorpyrifos alone and in conjunction with fluoride in rats
BACKGROUND/AIM: Chronic renal disorder is becoming a major health problem worldwide. The purpose of the present study was to investigate alterations in the renal antioxidant system in rats induced by repeated exposure to chlorpyrifos (CPF) alone and in conjunction with fluoride. MATERIALS AND METHODS: Wistar rats were randomly allocated to seven
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Cardiovascular dysfunction and oxidative stress following human contamination by fluoride along with environmental xenobiotics (Cd & Pb) in the phosphate treatment area of Togo, West Africa.
Highlights The exposure of the population is important in relation to the routes of exposure levels of pollutants. Cd, Pb and F in human blood are high in subjects living in and around the phosphate processing plant. The variation of the biochemical indicators indicating the risk of cardiovascular diseases. The
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Subchronic exposure to arsenite and fluoride from gestation to puberty induces oxidative stress and disrupts ultrastructure in the kidneys of rat offspring.
Highlights In utero and early life exposure to As and F affects kidney ultrastructure. Exposure to As and F alone or combined causes oxidative stress in kidney tissue. As exposure but not F alters the Nrf2 pathway-related signaling molecules. Concurrent As and F exposure may produce a joint action on
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WITHDRAWN: Co-exposure effects of arsenic and fluoride on intelligence and oxidative stress in school-aged children: a cohort study.
This article has been withdrawn at the request of the editor. The Publisher apologizes for any inconvenience this may cause. as of November 6, 2020 Highlights Pioneer biomonitoring study on rural children to address As and F- co-exposure. High dental Fluorosis found in relation to urinary As and F- levels in
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A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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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,
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Annapolis: Water Fluoridation Linked to Death of Dialysis Patient
EVENING CAPITAL (Annapolis, Maryland) November 29, 1979 Fluoride Linked to Death by Mary Ann Kryzankowicz Staff Writer Fluoride poisoning has been definitely linked to the death of a 65-year-old kidney dialysis patient who became ill during a blood cleaning process Nov 11. State Medical Examiner Dr. (illegible) Guard has ruled that Lawrence Blake, 65, of Arundel
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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
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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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