Human epidemiological studies showed that radon and arsenic exposures are major risk factors for lung cancer in Yunnan tin miners. However, biological evidence for this phenomenon is absent. In this study, HBE cells were exposed to different concentrations of sodium arsenite, different radon exposure times, or a combination of these two factors. The results showed a synergistic effect of radon and sodium arsenite in cell cytotoxicity as determined by cell viability. Elevated intracellular ROS levels and increased DNA damage indexed by comet assay and γ-H2AX were detected. Moreover, DNA HR repair in terms of Rad51 declined when the cells were exposed to both radon and sodium arsenite. The synergistic effect of radon and sodium arsenite in HBE cells may be attributed to the enhanced DSBs and inhibited HR pathway upon co-exposure.
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http://dx.doi.org/10.1016/j.etap.2015.11.013 | DOI Listing |
Environ Health Prev Med
January 2024
Health and Environmental Risk Division, National Institute for Environmental Studies.
Background: Chronic arsenite exposure has been known to induce cancer in various organs; however, the underlying mechanisms remain elusive. The characteristic feature of carcinogenesis due to arsenic exposure is that the disease develops after a prolonged latent period, even after cessation of exposure. Our previous study revealed that arsenite exposure induces premature senescence in hepatic stellate cells and suggests that the senescence-associated secretory phenotype (SASP) factors from the senescent cells promote hepatic carcinogenesis.
View Article and Find Full Text PDFApoptosis
December 2024
Department of Physiology, University of Calcutta, Kolkata, West Bengal, India.
Arsenic-mediated neurodegenerative disorders affect millions of individuals globally, but the specific impact of environmental arsenic on adult cerebellar degeneration and neurogenesis is incompletely understood. Of particular concern is arsenic-induced apoptosis-driven neurodegeneration. Our major objective was to investigate the molecular signaling intricacies associated with arsenic-induced death of cerebellar neurons and to propose folic acid as a possible intervention.
View Article and Find Full Text PDFChem Biol Interact
December 2024
Department of Environmental and Occupational Health, Sichuan University West China School of Public Health and West China Fourth Hospital, Chengdu, Sichuan, 610041, China. Electronic address:
Arsenic is a widespread environmental carcinogen, and its carcinogenic mechanism has been the focus of toxicology. N-methyladenosine (mA) binding protein YTH domain family protein 2 (YTHDF2) performs various biological functions by degrading mA-modified mRNAs. However, the mA-modified target mRNA of YTHDF2 in regulating arsenic carcinogenesis remains largely unknown.
View Article and Find Full Text PDFEcotoxicol Environ Saf
December 2024
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Baojian Road, Harbin, Heilongjiang 150081, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health of P. R. China, Harbin Medical University, Baojian Road, Harbin, Heilongjiang 150081, China. Electronic address:
Arsenic (As) can penetrate brain tissue through the blood-brain barrier (BBB), and the ATP-binding cassette subfamily B member 1 (Abcb1) has been shown to facilitate the transport of inorganic arsenic (iAs) in animal liver, small intestine, and yeast. However, the relationship between Abcb1 and BBB has not been reported, and the mechanism of brain microvascular endothelial cells Abcb1 on the transport of iAs needs to be further studied. Increased arsenic levels were observed in mice exposed to 25 mg/L or 50 mg/L of sodium arsenite (NaAsO) in drinking water, and both arsenic uptake and efflux were detected in bEnd.
View Article and Find Full Text PDFInt J Environ Health Res
December 2024
Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
This study examined the potential of vanillic acid (VA) to protect against renal oxidative stress and inflammation caused by sodium arsenite (SA) in mice. Mice were assigned to five groups: control, VA (100 mg/kg), SA (50 ppm in drinking water for 8 weeks), and SA + VA (50 and 100 mg/kg orally in the 7th and 8th weeks). After the experiment was ended, the Mice were sacrificed and serum and renal tissue samples were collected for additional assessments.
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