Regulation of autophagy in rat hepatocytes treated<i>in vitro</i>with low concentration of mercury

Chatterjee, Sarmishtha; Nandi, Pratyusha; Mukherjee, Sandip; Chattopadhyay, Ansuman; Bhattacharya, Shelley

doi:10.1080/02772248.2013.786941

Cited by 9 publications

(5 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Mercuric chloride damages cellular DNA by a nonapoptotic mechanism at a low dose (5 μM) in the U-937 cell line . Chatterjee et al , reported that 5 μM Hg toxicity drives autophagy following ATG5-ATG12-LC3B covalent-conjugation pathway modulation by Keap1-p62, ERK-p38, and DRAM-p53 regulator proteins through ubiquitination in rat hepatocytes. In addition, autophagy monitors cell fate in response to Hg, where Fas-associated death domain has been found to recruit one of the most important executioners of programmed cell death, caspase-8, to autophagosomes through interactions with ATG5 (Figure ).…”

Section: Mercury (Hg)mentioning

confidence: 99%

Toxic Metals and Autophagy

Chatterjee

Sarkar

Bhattacharya

2014

Chem. Res. Toxicol.

Self Cite

105

View full text Add to dashboard Cite

The earth's resources are finite, and it can no longer be considered a source of inexhaustible bounty for the human population. However, this realization has not been able to contain the human desire for rapid industrialization. The collateral to overusing environmental resources is the high-level contamination of undesirable toxic metals, leading to bioaccumulation and cellular damage. Cytopathological features of biological systems represent a key variable in several diseases. A review of the literature revealed that autophagy (PCDII), a high-capacity process, may consist of selective elimination of vital organelles and/or proteins that intiate mechanisms of cytoprotection and homeostasis in different biological systems under normal physiological and stress conditions. However, the biological system does survive under various environmental stressors. Currently, there is no consensus that specifies a particular response as being a dependable biomarker of toxicology. Autophagy has been recorded as the initial response of a cell to a toxic metal in a concentration- and time-dependent manner. Various signaling pathways are triggered through cellular proteins and/or protein kinases that can lead to autophagy, apoptosis (or necroptosis), and necrosis. Although the role of autophagy in tumorigenesis is associated with promoting tumor cell survival and/or acting as a tumor suppressive mechanism, PCDII in metal-induced toxicity has not been extensively studied. The aim of this review is to analyze the comparative cytotoxicity of metals/metalloids and nanoparticles (As, Cd, Cr, Hg, Fe, and metal-NP) in cells enduring autophagy. It is noted that metals/metalloids and nanoparticles prefer ATG8/LC3 as a potent inducer of autophagy in several cell lines or animal cells. MAP kinases, death protein kinases, PI3K, AKT, mTOR, and AMP kinase have been found to be the major components of autophagy induction or inhibition in the context of cellular responses to metals/metalloids and nanoparticles.

show abstract

Section: Mercury (Hg)mentioning

confidence: 99%

Toxic Metals and Autophagy

Chatterjee

Sarkar

Bhattacharya

2014

Chem. Res. Toxicol.

Self Cite

105

View full text Add to dashboard Cite

show abstract

“…It is difficult to detect elongated monomeric form of these proteins to complete autophagic vacuole formation Suzuki et al 2001;Hanada et al 2007). Chatterjee et al (2012Chatterjee et al ( , 2013a recently demonstrated that ATG5-ATG12 complex facilitates LC3B mediated autophagy in Hgtreated differentiated hepatocytes within 30 min of incubation and continued until 4 hr. However, the present study demonstrated significant involvement of ATG12, LC3B, and BCL2 proteins in Hg-induced oval cell death.…”

Section: Discussionmentioning

confidence: 98%

“…10, 1722-1738, http://dx.doi.org/10.1080/02772248.2014 both eukaryotic and prokaryotic cells (Schurz, Sabater-Vilar, and Fink-Gremmels 2000). The characteristic changes in cellular level are protein precipitation, enzyme inhibition, cell swelling, nuclear degradation, ATP depletion, and mitochondrial damage (Ben-Ozer et al 2000;Patnaik et al 2010;Schlatter et al 2011;Chatterjee et al 2012Chatterjee et al , 2013aChatterjee et al , 2013b. These pathological conditions drive cytotoxicity towards different types of programed cell death (Ben-Ozer et al 2000;Ung et al 2010;Chatterjee et al 2013b).…”

Section: Introductionmentioning

confidence: 95%

“…Toxicity varies with the form of Hg, dose, and rate of exposure which, in extreme cases, may be fatal (Berlin, Zalups, and Fowler 2007). Low-grade chronic exposure to elemental or other forms of Hg induces oxidative stress (Ben-Ozer et al 2000;Patnaik et al 2010;Chatterjee et al 2013a), neurotoxicity (Ni et al 2012), gastrointestinal distress (Berlin, Zalups, and Fowler 2007), and immune dysfunction (Sweet and Zelikoff 2001). Moreover, Hg exposure may produce liver injury that may lead to other syndromes (Ung et al 2010 Toxicological & Environmental Chemistry, 2013Vol.…”

Section: Introductionmentioning

confidence: 97%

See 1 more Smart Citation

Mercuric chloride effects on adult rat oval cells-induced apoptosis

Chatterjee

Munshi

Chattopadhyay

et al. 2013

Toxicological & Environmental Chemistry

Self Cite

View full text Add to dashboard Cite

In the present investigation, the toxicity of mercuric chloride (HgCl 2 ) was evaluated in adult oval cells isolated from rat utilizing the 2-acetylaminofluorene/partial hepatectomy technique. Isolated oval cells were incubated with 5 mM of HgCl 2 for 8 hr to elucidate in vitro cytotoxic responses. Recently, autophagic cell death was found in rat hepatocytes in vitro within 30 min of incubation with 5 mM of mercury (Hg) which triggered apoptosis and necroptosis in a time-dependent manner. Nuclear degradation occurred within 30 min of incubation and progressed with time until 8 hr. Apoptosis evidenced by activation of caspase-dependent pathway between 30 min to 8 hr of incubation was mediated via interchange of death domain signaling pathways. Receptor-interacting protein played a positive role to modulate the death domain receptors in the scenario of apoptotic death of oval cells until 6 hr. Autophagic marker proteins ATG12 and LC3B exerted a significant role in triggering apoptosis in 5 mM Hg-treated oval cells. No apparent expression of apoptosis-inducing-factor (AIF) and HMGB1 indicated absence of caspase-independent apoptosis and necrosis in the rat oval cells between 30 min and 8 hr. Thus a low concentration of Hg modulates programmed cell death in adult rat oval cells by altering expression of proteins involved in the molecular mechanisms of cellular functions.

show abstract

“…Aliás, a exposição mercurial também é hepatotóxica, induzindo morte celular e autofagia em células do fígado (hepatócitos) 26,52 . Além dos efeitos supracitados, o mercúrio prejudica o sistema reprodutor de mamíferos.…”

Section: Outros Efeitos Do Mercúrio Sobre a Saúde Humanaunclassified

Mercúrio e Amálgama Odontológico: Implicações para a Saúde Coletiva

Prampero¹,

Rubin

Prampero

2016

Saúde E Desenvolvimento Humano

View full text Add to dashboard Cite

Resumo:A contaminação ambiental e as exposições ocupacionais por mercúrio estão relacionadas a diversos problemas de saúde desde o período fetal. Pelo fato do amálgama ser um material restaurador amplamente usado em odontologia, em virtude da sua facilidade de utilização e do baixo custo, o objetivo deste trabalho foi elaborar uma revisão bibliográfica sobre os aspectos ambientais, ocupacionais e toxicológicos da contaminação mercurial. Foi realizada uma revisão utilizando as bases de dados Medline, ISI e LILACS cobrindo o período de 2004 a 2015. O mercúrio está relacionado à redução do crescimento ponderal e desenvolvimento cognitivo de crianças, bem como a distúrbios psico-afetivos, autismo, doença de Alzheimer, infertilidade masculina e problemas cardiometabólicos. Embora a contribuição das amálgamas dentárias para a liberação de mercúrio não seja tão expressiva comparada à contaminação por atividades de garimpo e outras fontes, seu uso deve começar a ser restrito para reduzir as emissões de mercúrio. Abstract:Environmental pollution and occupational exposures by Mercury have been associated with many health problems since the fetal life. Since amalgam is widely used in dentistry due to its ease use and lower cost, the objective of this work was to elaborate a review regarding Mercury pollution and environmental, occupational and health aspects. A review covering 2010 to 2014 period using Medline, ISI, and LILACS databases were done. Mercury is associated with reduction of physical growth and cognitive development in children as well as psycho-affective disturbancies, autism, Alzheimer's disease, male infertility, and cardiometabolic problems. Although the amagalm contribution to Mercury release is not so relavant as compared to gold-mining and other sources its use should beggin to be restricted in order to reduce Mercury emissions.

show abstract

Regulation of autophagy in rat hepatocytes treatedin vitrowith low concentration of mercury

Cited by 9 publications

References 33 publications

Toxic Metals and Autophagy

Toxic Metals and Autophagy

Mercuric chloride effects on adult rat oval cells-induced apoptosis

Mercúrio e Amálgama Odontológico: Implicações para a Saúde Coletiva

Contact Info

Product

Resources

About