Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Gao, Yan; Liang, Chen; Zhang, Jianhai; Ma, Junjie; Wang, Jinming; Niu, Ruiyan; Tikka, Chiranjeevi; Wang, Yewei

doi:10.1159/000494239

Cited by 13 publications

(4 citation statements)

References 38 publications

(46 reference statements)

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“…Recently it has been shown that co-exposures with fluoride with sulfur dioxide worsen on brain and kidney toxicity [73, 74]. In this study, similar alterations in spermatozoa quality, mitochondrial impaired function, apoptosis increasing have previously evidenced in the fluoride and diabetes exposure at reproductive level; however, their combination aggravates the spermatozoa function.…”

Section: Discussionsupporting

confidence: 78%

Exposure of Fluoride with Streptozotocin-Induced Diabetes Aggravates Testicular Damage and Spermatozoa Parameters in Mice

Sánchez-Gutiérrez

Martinez-Loredo

Madrigal-Santillán

et al. 2019

Journal of Toxicology

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Diabetes mellitus is the most common chronic disease worldwide that causes numerous complications, including male infertility. The prevalence of DM is 451 million people and estimated that would increase to 693 million in 2045. Fluorosis caused by drinking water contaminated with inorganic fluoride is a public health problem in many areas around the world. Previous studies have shown that fluoride exposure damages the male reproductive function. This study aimed to evaluate the fluoride sub-chronic exposure on the spermatozoa function in streptozotocin (STZ)-induced diabetic mice. After confirming diabetes by measuring blood glucose levels, the male mice received 45.2 ppm of fluoride added or deionized water. We evaluated several parameters in diabetic mice exposed to fluoride: standard quality analysis, the mitochondrial transmembrane potential (ψm), the caspase activity in spermatozoa, urinary fluoride excretion, and histological evaluation in the testes. After 60 days of fluoride-exposure, diabetic mice, significantly decreased sperm quality (motility, viability, and concentration). Spermatozoa from fluoride-exposure in diabetic mice presented a significant decrease in ψm and a significant increase in activity caspase 3/7. Urinary fluoride excretion was decreased in diabetic mice exposed to fluoride. Subchronic fluoride exposure of mice with STZ-induced diabetes aggravated testicular damage and the spermatozoa function.

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Section: Discussionsupporting

confidence: 78%

Exposure of Fluoride with Streptozotocin-Induced Diabetes Aggravates Testicular Damage and Spermatozoa Parameters in Mice

Sánchez-Gutiérrez

Martinez-Loredo

Madrigal-Santillán

et al. 2019

Journal of Toxicology

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“…As the primary organ that eliminates wastes from the body, the kidney is particularly susceptible to the effects of environmental toxins [40]. For example, previous animal studies suggested that inhaling of SO 2 can lead to renal tissue lesions, induce oxidative stress responses, and cause dose-dependent increases in DNA injuries in kidney [40][41][42]. In addition to inflammation responses, one study found that O 3 inhalation can modify the gene expression in rat's kidney, e.g.…”

Section: Discussionmentioning

confidence: 99%

Associations of long-term exposure to ambient sulfur dioxide, carbon monoxide, ozone, and benzene with risk of incident chronic kidney disease in the UK

Zhang,

Liu,

Yang

et al. 2024

Environ. Res. Lett.

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Background.Limited studies have examined associations of gaseous air pollutants exposure with chronic kidney disease (CKD) in Europe. This study aimed to calculate the relationships between long-term exposure to ambient sulfur dioxide (SO2), carbon monoxide (CO), ozone (O3), and benzene and CKD in the UK.Methods.We included 502,369 participants from the UK biobank cohort. Associations of SO2, CO, O3, and benzene with CKD were estimated using Cox proportional hazards model. The shape of the exposure-response association between each air pollutant and CKD was then depicted using the shape constrained health impact function. We finally estimated the incidence of CKD attributable to each air pollutant by linking the constructed exposure-response association to the 2019 Global Burden of Disease data.Results.Our results suggested SO2, high O3 days (daily max 8-hr O3 concentration > 120 µg/m3), CO, and benzene were positively associated with the risk of incident CKD. The HRs of CKD for SO2, CO, and benzene were 1.058 (95%CI: 1.039-1.078), 1.003 (95%CI: 1.001-1.005), and 1.619 (1.433-1.829) for every 1 µg/m3 increase in the concentration, respectively. For high O3 days, the HR of CKD was 1.044 (95%CI: 1.032-1.056) for every 1 day increase, but correlation to O3 concentration did not to reach the statistical significance in the time-varying model. The risk of CKD increased non-linearly with increasing SO2, high O3 days, and CO, and linearly with increasing benzene. We estimated that 7.9%, 16.0%, 8.0% of incident CKD cases in the UK in 2021 could be attributed to exposure to SO2, O3, and benzene, respectively.Conclusions.Exposure to SO2, CO, O3, and benzene were all positively associated with increased CKD risk. Our findings highlight the importance of considering air pollution while making strategies targeting on CKD management.

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“…A large amount of fluoride deposition mainly damages to bones, teeth, and central nervous system via passing through the blood-brain barrier that can lead to insomnia or somnolence and other symptoms ( 12 ). There is evidence that excessive fluoride intake can damage various organs including brain ( 13 , 14 ), liver ( 15 , 16 ), kidney ( 17 ), ovary ( 18 ). Fluoride in the environment into the body is mainly absorbed by the stomach and intestines, through the cell membrane, deposited in bone and soft tissue, causing damage to bone and soft tissue.…”

Section: Introductionmentioning

confidence: 99%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.

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Combination of Fluoride and SO2 Induce DNA Damage and Morphological Alterations in Male Rat Kidney

Cited by 13 publications

References 38 publications

Exposure of Fluoride with Streptozotocin-Induced Diabetes Aggravates Testicular Damage and Spermatozoa Parameters in Mice

Exposure of Fluoride with Streptozotocin-Induced Diabetes Aggravates Testicular Damage and Spermatozoa Parameters in Mice

Associations of long-term exposure to ambient sulfur dioxide, carbon monoxide, ozone, and benzene with risk of incident chronic kidney disease in the UK

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

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