Mechanisms pertaining to arsenic toxicity

Singh, Amrit Pal; Goel, Rajesh Kumar; Kaur, Tajpreet

doi:10.4103/0971-6580.84258

Cited by 237 publications

(67 citation statements)

References 71 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…7 The toxicity of arsenic can be attributed to the ability of this metallic element to react with sulfhydryl proteins, which causes the activity to shift in some cell signaling pathways, in particular, the mitogen-activated protein kinases. 8 Another mechanism involved in the toxicity of arsenic is the stimulation of the generation of free radicals and the induction of oxidative stress. 8 Oxidative stress status is an imbalance between the production of active oxygen species and the ability of a biological system to eliminate these compounds, which results in damage to the biological system and consequently organ dysfunction.…”

Section: Introductionmentioning

confidence: 99%

“…8 Another mechanism involved in the toxicity of arsenic is the stimulation of the generation of free radicals and the induction of oxidative stress. 8 Oxidative stress status is an imbalance between the production of active oxygen species and the ability of a biological system to eliminate these compounds, which results in damage to the biological system and consequently organ dysfunction. 8,9 Oxidative stress is one of the ways of the main causes of renal failure.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Histopathological Changes and Antioxidant Enzymes Status in Oxidative Stress Induction Using Sodium arsenite in Rats

Nozohour

Jalilzadeh-Amin

2019

J Apple Biotechnol Rep

View full text Add to dashboard Cite

Introduction: Arsenic toxicity has posed troublesome health concerns in the world and many of the toxic effects of arsenic are related to its effect on oxidative stress. The aim of the present study is to evaluate histopathological and antioxidant enzymes changes in oxidative stress status induced by sodium arsenite in rats. Materials and Methods: All experiments were carried out in male Wistar rats. Animal were divided into 2 groups of eight animals in each: Rats consumed distilled water (control group). Group 2: Rats consumed a solution of sodium arsenite (100 ppm) daily (arsenic group). At the end of day 28 arsenic exposure, the enzyme level in rat liver and kidney tissues was measured using the assay kits. The remaining liver, kidney, and heart tissue were fixed in 10% neutral-buffered formalin and used for histological observation. Results: The results showed a significant decrease in values of glutathione peroxidase (GPx), superoxide dismutase (SOD), total antioxidant capacity (TAC) and catalase (CAT) in serum and tissue in kidney and liver rat (P < 0.05). But, malondialdehyde (MDA) levels were increased significantly (P < 0.05). Arsenic caused severe degenerative changes in tubular cells and acute tubular necrosis, hepatocyte cell degeneration, severe hemorrhage, and infiltration and formation of Kupffer cells nodules, fragmentation, and degeneration of muscle fibers with pyknotic nuclei in heart tissue. Conclusions: The finding of the present study revealed that the administration of Sodium arsenite caused significant oxidative stress, decreased antioxidant enzymes activity and severe tissue damage.

show abstract

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Histopathological Changes and Antioxidant Enzymes Status in Oxidative Stress Induction Using Sodium arsenite in Rats

Nozohour

Jalilzadeh-Amin

2019

J Apple Biotechnol Rep

View full text Add to dashboard Cite

show abstract

“…Exposure to arsenic has been associated with cancer, diabetes, cardiovascular disease, and metabolic syndrome (Singh et al 2011, Maull et al 2012, Kim et al 2015, Mohammed Abdul et al 2015). It has been suggested that arsenic alters common pathways such as those involved in oxidative stress and inflammatory signaling, which underlie a variety of arsenic-associated diseases (States et al 2009, Straif et al 2009, Mo et al 2011, Kim et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells

Pace

Banerjee

Welch

et al. 2016

Toxicology in Vitro

View full text Add to dashboard Cite

Arsenic exposure has been implicated as a risk factor for cardiovascular diseases, metabolic disorders, and cancer, yet the role mitochondrial dysfunction plays in the cellular mechanisms of pathology is largely unknown. To investigate arsenic-induced mitochondrial dysfunction in vascular smooth muscle cells (VSMCs), we exposed rat aortic smooth muscle cells (A7r5) to inorganic arsenic (iAs(III)) and its metabolite monomethylarsonous acid (MMA(III)) and compared their effects on mitochondrial function and oxidative stress. Our results indicate that MMA(III) is significantly more toxic to mitochondria than iAs(III). Exposure of VSMCs to MMA(III), but not iAs(III), significantly decreased basal and maximal oxygen consumption rates and concomitantly increased compensatory extracellular acidification rates, a proxy of glycolysis. Treatment with MMA(III) significantly increased hydrogen peroxide and superoxide levels compared to iAs(III). Exposure to MMA(III) resulted in significant decreases in mitochondrial ATP, aberrant perinuclear clustering of mitochondria, and decreased mitochondrial content. Mechanistically, we observed that mitochondrial superoxide and hydrogen peroxide contribute to mitochondrial toxicity, as treatment of cells with MnTBAP (a mitochondrial superoxide dismutase mimetic) and catalase significantly reduced mitochondrial respiration deficits and cell death induced by both arsenic compounds. Overall, our data demonstrates that MMA(III) is a mitochondria-specific toxicant that elevates mitochondrial and non-mitochondrial sources of ROS.

show abstract

“…Discovering new risk factors and confirming suspicions is difficult as there is typically a long latency period from time of exposure to the development of cancer and environmental carcinogens may occur together, limiting the ability to identify the risk posed by each individual exposure. Arsenic contamination in drinking water is a worldwide concern and remains a considerable cancer risk factor in many countries including Bangladesh, Taiwan, India, Mexico, China, Chile, Argentina and the USA (74). By far, arsenic in drinking water poses the greatest threat to human health (17, 75).…”

Section: Discussionmentioning

confidence: 99%

Involvement of Epigenetics and EMT-Related miRNA in Arsenic-Induced Neoplastic Transformation and Their Potential Clinical Use

Michailidi

Hayashi

Datta

et al. 2015

Cancer Prevention Research

View full text Add to dashboard Cite

Exposure to toxicants leads to cumulative molecular changes that overtime increase a subject’s risk of developing urothelial carcinoma (UC). To assess the impact of arsenic exposure at a time progressive manner, we developed and characterized a cell culture model and tested a panel of miRNAs in urine samples from arsenic exposed subjects, UC patients and controls. To prepare an in vitro model, we chronically exposed an immortalized normal human bladder cell line (HUC1) to arsenic. Growth of the HUC1 cells was increased in a time dependent manner after arsenic treatment and cellular morphology was changed. In soft agar assay, colonies were observed only in arsenic treated cells and the number of colonies gradually increased with longer periods of treatment. Similarly, invaded cells in invasion assay were observed only in arsenic treated cells. Withdrawal of arsenic treatment for 2.5 months did not reverse the tumorigenic properties of arsenic treated cells. Western blot analysis demonstrated decreased PTEN and increased AKT and mTOR in arsenic treated HUC1 cells. Levels of miR-200a, miR-200b, and miR-200c were down-regulated in arsenic exposed HUC1 cells by quantitative RT-PCR. Furthermore, in human urine, miR-200c and miR-205 were inversely associated with arsenic exposure (P=0.005 and 0.009, respectively). Expression of miR-205 discriminated cancer cases from controls with high sensitivity and specificity (AUC=0.845). Our study suggests that exposure to arsenic rapidly induces a multifaceted dedifferentiation program and miR-205 has potential to be used as a marker of arsenic exposure as well as a maker of early UC detection.

show abstract

Mechanisms pertaining to arsenic toxicity

Cited by 237 publications

References 71 publications

Histopathological Changes and Antioxidant Enzymes Status in Oxidative Stress Induction Using Sodium arsenite in Rats

Histopathological Changes and Antioxidant Enzymes Status in Oxidative Stress Induction Using Sodium arsenite in Rats

Monomethylarsonous acid, but not inorganic arsenic, is a mitochondria-specific toxicant in vascular smooth muscle cells

Involvement of Epigenetics and EMT-Related miRNA in Arsenic-Induced Neoplastic Transformation and Their Potential Clinical Use

Contact Info

Product

Resources

About