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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Arsenic and fluoride co-exposure through drinking water and their impacts on intelligence and oxidative stress among rural school-aged children of Lahore and Kasur districts, Pakistan.
Arsenic (As), and fluoride (F-) are potent contaminants with established carcinogenic and non-carcinogenic impacts on the exposed populations globally. Despite elevated groundwater As and F- levels being reported from various regions of Pakistan no biomonitoring study has been reported yet to address the co-exposure impact of As and F- among
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Toxic effects of deltamethrin and fluoride on antioxidant parameters in rats.
Toxic effects of the pyrethroid pesticide deltamethrin and water-borne fluoride, alone and in combination, on free radical mediated parameters are reported in rats. Twenty-four healthy adult Wistar rats of both sexes were divided into 4 groups with 6 rats in each group. Group I receiving no treatment served as the
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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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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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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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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
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