Fluoride enhances generation of reactive oxygen and nitrogen species, oxidizes hemoglobin, lowers antioxidant power and inhibits transmembrane electron transport in isolated human red blood cells

Maheshwari, Nikhil; Qasim, Neha; Anjum, Rubi

doi:10.1016/j.ecoenv.2020.111611

Cited by 34 publications

(15 citation statements)

References 51 publications

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“…However, drinking water, foodstuffs, and fluoride-containing dental products are currently considered major contributed products to the increased fluoride intake in the human organism. Among the above, most of the scientific evidence confirms the fact that drinking water is the main and major source of human exposure to fluorides [7,24,[36][37][38][39][40]. The amount of fluoride in groundwater is determined by heterogeneous factors, including the soil through which the water leaches, agricultural production practices, the proximity of factories, the type of water pipes used, the population of the area, and many more.…”

Section: Resultsmentioning

confidence: 99%

Deterministic and probabilistic human health risk assessment for fluorides in drinking groundwater from Lukavac, Bosnia and Herzegovina

Husejnović¹,

Turkić

Halilčević

et al. 2022

Environ Anal Health Toxicol

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Although fluorides are essential for dental health, there are growing health concerns regarding the risk-benefit ratio of fluoride exposure. The objectives of the study were to obtain data on the amount and human health risks of fluoride in drinking groundwater, as well as to compare and evaluate the differences in the outputs obtained by two different approaches in health risk assessment (deterministic vs probabilistic). From a densely populated industrial area of north-eastern Bosnia and Herzegovina, a total of 54 groundwater samples were collected. Fluoride concentrations varied from 1.69 to 3.52 mg/L. The WHO's threshold value for fluoride in drinking water was exceeded in all the samples analysed, indicating an increased daily intake of fluoride from groundwater. Deterministic and semi-probabilistic techniques were used for exposure assessment and health risk quantification. Generally, the deterministic approach resulted in acceptable health risks in most adult exposure scenarios. However, the Monte Carlo simulation revealed that 20.6, 20.8, and 99.8% of adult males, females, and children, respectively, were above the tolerable upper intake level, indicating that both adults and children face a significant health risk. Nevertheless, small children are more vulnerable to environmental hazards than youth and adults. Hence, a more in-depth risk-benefit analysis is required to reduce/or optimize fluoride content in drinking water to prevent tooth decay and fluorosis at all ages. Considering that optimal daily intake of fluorides is a crucial factor for preserving human health, decision-makers should take steps to emphasize the importance of continuous monitoring of fluoride concentrations in drinking water.

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Section: Resultsmentioning

confidence: 99%

Deterministic and probabilistic human health risk assessment for fluorides in drinking groundwater from Lukavac, Bosnia and Herzegovina

Husejnović¹,

Turkić

Halilčević

et al. 2022

Environ Anal Health Toxicol

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“…Also, ZO addition ameliorated toxicant brought about signi cant reduction in NO levels in contrast quercetin was less effective in restoring NO levels in the combination toxicant group. Exposure to F − stimulates ROS production and the ensuing oxidative stress hampers antioxidant enzyme activity, energy metabolism and ion transport across plasma membranes [54]. Acute fatal F − toxicity diminishes calcium ionic concentration in blood which affects contractability of cardiac cells causing cardiac arrest [55], whereas prolonged exposure to F − leads to electrolyte imbalance with signi cant reduction of Ca and magnesium levels in plasma [56].…”

Section: Discussionmentioning

confidence: 99%

Oxidative renal damage induced by fluoride and dimethoate and its mitigation by Zingiber officinale in Wistar rats

Sharma

Verma

Sood

et al. 2022

Preprint

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Simultaneous exposure of dimethoate (DM) and fluoride (F−) is a natural phenomenon which may insidiously impact functioning of various organs including kidney. Zingiber officinale (ZO) is harbours excellent natural antioxidant properties. Therefore, the present investigation was aimed to determine the potential of ZO in alleviating renal oxidative damage induced by DM and F− alone and by their concurrent exposure in Wistar rats. Subacute toxicity study was conducted on fifty four Wistar rats randomly allocated to nine groups with six rats in each. Following sub-acute exposure of either F− or DM a significant rise in blood urea nitrogen, creatinine and uric acid along with a significant declined in plasma levels of reduced glutathione and nitric oxide occurred. Significantly declined total antioxidant status, total thiols, catalase, superoxide dismutase, glutathione peroxidase, aryl esterase and acetylcholinesterase in renal tissue with increased levels of lipid and protein peroxidation were recorded alongside pathological alterations in renal tissue of toxicant exposed rats as compared to control. However, more severe changes were observed in levels of the above biomarkers and renal histoarchitecture on co-administration of both the toxicants indicating enhanced toxicity. Concurrent exposures of ZO extract along with either or both the toxicants led to significant restoration of activities of the antioxidant apparatus, biochemical profile of kidney and renal histology. Hence, repeated administration of ZO extract alongside individual as well as dual toxicant treatment caused amelioration of oxidative damage, renal biomarkers and histopathological alterations in renal tissue of Wistar rats.

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“…Fluoride-induced oxidative stress has been correlated to iron metabolism disorders, which are characterized by increased iron and hepcidin levels, but decreased expression of iron transporters ( Niu et al, 2018 ). In vitro experiments found that human red blood cells treated with NaF produced methemoglobin and oxyhemoglobin, with increased heme degradation, resulting in the release of free iron from porphyrin rings ( Maheshwari et al, 2021 ). These findings suggested that fluoride exposure may have a potential impact on iron metabolism.…”

Section: Relationship Between Fluorosis and Ferroptosismentioning

confidence: 99%

Prospects for the Role of Ferroptosis in Fluorosis

Zhang

Jiang

et al. 2021

Front. Physiol.

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As a strong oxidant, fluorine can induce oxidative stress resulting in cellular damage. Ferroptosis is an iron-dependent type of cell death caused by unrestricted lipid peroxidation (LPO) and subsequent plasma membrane rupture. This article indicated a relationship between fluorosis and ferroptosis. Evidence of the depletion of glutathione (GSH) and increased oxidized GSH can be found in a variety of organisms in high fluorine environments. Studies have shown that high fluoride levels can reduce the antioxidant capacity of antioxidant enzymes, while increasing the contents of reactive oxygen species (ROS) and malondialdehyde (MDA), resulting in oxidative stress and fluoride-induced oxidative stress, which are related to iron metabolism disorders. Excessive fluorine causes insufficient GSH, glutathione peroxidase (GSH-Px) inhibition, and oxidative stress, resulting in ferroptosis, which may play an important role in the occurrence and development of fluorosis.

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Fluoride enhances generation of reactive oxygen and nitrogen species, oxidizes hemoglobin, lowers antioxidant power and inhibits transmembrane electron transport in isolated human red blood cells

Cited by 34 publications

References 51 publications

Deterministic and probabilistic human health risk assessment for fluorides in drinking groundwater from Lukavac, Bosnia and Herzegovina

Deterministic and probabilistic human health risk assessment for fluorides in drinking groundwater from Lukavac, Bosnia and Herzegovina

Oxidative renal damage induced by fluoride and dimethoate and its mitigation by Zingiber officinale in Wistar rats

Prospects for the Role of Ferroptosis in Fluorosis

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