Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by dietary phosphate

Majumdar, Sangita; Karmakar, Subhra; Maiti, Anasuya; Choudhury, Monalisa; Ghosh, Aniruddha; Das, Asankur Sekhar; Mitra, Chandan

doi:10.1016/j.etap.2010.09.011

Cited by 21 publications

(7 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increased production of ROS associated with enhanced lipid peroxidation and decreased levels of reduced glutathione, the activity of superoxide dismutase and catalase as observed in the present study consistent with the earlier findings [20,21]. Most of the toxic chemicals directly act on the mitochondria, disrupt its phospholipids membrane and cause mitochondrial dysfunctions [2,52,53]. Arsenic compounds have been shown to be strong inducers of apoptosis in normal and transformed cells through production of ROS [54], decreased mitochondrial membrane potential [52], activation of caspases [25,55], increased fragmentation of DNA [55], decreased expression of anti-apoptotic proteins (Bcl-2, Bcl-XL) and increased expression of pro-apoptotic proteins [55].…”

Section: Discussionsupporting

confidence: 92%

Immunomodulatory role of Emblica officinalis in arsenic induced oxidative damage and apoptosis in thymocytes of mice

Singh

Yadav

Gupta

et al. 2013

BMC Complement Altern Med

View full text Add to dashboard Cite

BackgroundArsenic is widely distributed in the environment and has been found to be associated with the various health related problems including skin lesions, cancer, cardiovascular and immunological disorders. The fruit extract of Emblica officinalis (amla) has been shown to have anti-oxidative and immunomodulatory properties. In view of increasing health risk of arsenic, the present study has been carried out to investigate the protective effect of amla against arsenic induced oxidative stress and apoptosis in thymocytes of mice.MethodsMice were exposed to arsenic (sodium arsenite 3 mg/kg body weight p.o.) or amla (500 mg/kg body weight p.o.) or simultaneously with arsenic and amla for 28 days. The antioxidant enzyme assays were carried out using spectrophotometer and generation of ROS, apoptotic parameters, change in cell cycle were carried out using flow cytometer following the standard protocols.ResultsArsenic exposure to mice caused a significant increase in the lipid peroxidation, ROS production and decreased cell viability, levels of reduced glutathione, the activity of superoxide dismutase, catalase, cytochrome c oxidase and mitochondrial membrane potential in the thymus as compared to controls. Increased activity of caspase-3 linked with apoptosis assessed by the cell cycle analysis and annexin V/PI binding was also observed in mice exposed to arsenic as compared to controls. Co-treatment with arsenic and amla decreased the levels of lipid peroxidation, ROS production, activity of caspase-3, apoptosis and increased cell viability, levels of antioxidant enzymes, cytochrome c oxidase and mitochondrial membrane potential as compared to mice treated with arsenic alone.ConclusionsThe results of the present study exhibits that arsenic induced oxidative stress and apoptosis significantly protected by co-treatment with amla that could be due to its strong antioxidant potential.

show abstract

Section: Discussionsupporting

confidence: 92%

Immunomodulatory role of Emblica officinalis in arsenic induced oxidative damage and apoptosis in thymocytes of mice

Singh

Yadav

Gupta

et al. 2013

BMC Complement Altern Med

View full text Add to dashboard Cite

show abstract

“…This result is in accordance with the previous studies using arsenic and other toxicity in the liver [37,39]. This may be due to As-induced free radical damage in the lipid membrane of hepatocytes seep out these enzymes in the cytosol released into the bloodstream which indicate the liver damage [40]. However, preadministration of SFN remarkably improved these altered hepatic markers by arsenic via its membrane-stabilization properties against ROS-mediated oxidative hepatic injury [41].…”

Section: Discussionsupporting

confidence: 91%

Sulforaphane Potentially Ameliorates Arsenic Induced Hepatotoxicity in Albino Wistar Rats: Implication of PI3K/Akt/Nrf2 Signaling Pathway

Thangapandiyan

Ramesh

Hema

et al. 2019

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…MtDNAcn is related to the size and number of mitochondria (Lee and Wei, 2005), which can alter under different energy demands. Experimental studies have reported that exposure to As was related to reduced Ca 2+ -ATPase activity (Majumdar et al, 2011;Muthumani and Miltonprabu, 2015), which led to decrease in energy production. Increases in energy demands can overwhelm the mitochondria and result in decreased mtDNAcn.…”

Section: Discussionmentioning

confidence: 99%

Exposure to arsenic during pregnancy and newborn mitochondrial DNA copy number: A birth cohort study in Wuhan, China

et al. 2020

View full text Add to dashboard Cite

Background: Arsenic (As) is a widely distributed environmental chemical with potentially different toxicities. However, little is known about the impact of maternal As exposure on newborn mitochondrial DNA copy number (mtDNAcn), which may lie on the pathway linking As exposure to adverse health impacts. Objectives:We aimed to explore whether maternal As exposure was associated with newborn mtDNAcn. Methods:We conducted a birth cohort study of 762 mother-infant pairs in Wuhan, China, 2013-2015. Cord blood mtDNAcn was determined using qPCR. Maternal urinary As levels in each trimester were quantified by ICP-MS. Multiple informant models were used to examine the associations of repeated urinary As levels with cord blood mtDNAcn. Results:The median urinary As levels in the first, second, and third trimesters were 17.2 g/L, 16.0 g/L and 17.0 g/L respectively. In the multivariate model, each doubling increase in the first-trimester urinary As level was associated with a 6.6% (95% CI: -12.4%, -0.5%) decrease in cord blood mtDNAcn. The highest versus lowest quintile of first-trimester urinary As level was related to a 19.0% (95% CI:-32.9%, -2.2%) lower cord blood mtDNAcn. There was significant association of urinary As levels in the second and third trimesters with cord blood mtDNAcn. The inverse relationship between first-trimester urinary As level and cord blood mtDNAcn was more pronounced among female infants.Conclusions: First-trimester As exposure was associated with decreased cord blood mtDNAcn. The potential health impacts of decreased mtDNAcn in early life need to be further clarified.

show abstract

Arsenic-induced hepatic mitochondrial toxicity in rats and its amelioration by dietary phosphate

Cited by 21 publications

References 45 publications

Immunomodulatory role of Emblica officinalis in arsenic induced oxidative damage and apoptosis in thymocytes of mice

Immunomodulatory role of Emblica officinalis in arsenic induced oxidative damage and apoptosis in thymocytes of mice

Sulforaphane Potentially Ameliorates Arsenic Induced Hepatotoxicity in Albino Wistar Rats: Implication of PI3K/Akt/Nrf2 Signaling Pathway

Exposure to arsenic during pregnancy and newborn mitochondrial DNA copy number: A birth cohort study in Wuhan, China

Contact Info

Product

Resources

About