Present study examined the genotoxic effects of arsenite in ovarian tissue of rat at 56 days of age. Immature (28 days old) female rats were exposed to different doses (50, 100, and 200 ppm) of sodium arsenite in drinking water for 28 days. DNA damage in ovarian tissue was measured by comet assay. All doses induced significant decrease in ovarian weight in a dose-dependent manner compared to control, more prominently at (P<0.001) 100 and 200 ppm. All the comet assay parameters showed significant difference with arsenite treatment compared to control group. In treatment groups, mean number of cells with intact DNA decreased while, mean comet number increased (P<0.001) in a dose-dependent manner compared to control. Significant decrease (P<0.05) was observed in mean comet length, height, comet head diameter and %DNA in comet head of high dose groups compared to control group. Dose dependent increase was found in mean comet tail length, %DNA in tail, tail moment and olive tail moment in high dose groups compared to control group. The study indicates that arsenic caused DNA damage to ovarian cells particularly at high doses and ensure comet assay as an effective method to detect DNA damage in tissue caused by metals.
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http://dx.doi.org/10.1016/j.toxlet.2009.07.003 | DOI Listing |
Apoptosis
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.
View Article and Find Full Text PDFNeurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) are characterized by complex etiologies, often involving disruptions in functions of RNA/DNA binding proteins (RDBPs) such as FUS and TDP-43. The cytosolic mislocalization and aggregation of these proteins are linked to accumulation of unresolved stress granules (SGs), which exacerbate the disease progression. Poly-ADP-ribose polymerase (PARP)-mediated PARylation plays a critical role in this pathological cascade, making it a potential target for intervention.
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