Autophagy as an ultrastructural marker of heavy metal toxicity in human cord blood hematopoietic stem cells

Gioacchino, Mario Di; Petrarca, Claudia; Perrone, Angela; Farina, Massimo; Sabbioni, E.; Hartung, Thomas; Martino, Simone; Esposito, Diana L.; Lotti, Lavinia Vittoria; Mariani-Costantini, Renato

doi:10.1016/j.scitotenv.2007.11.009

Cited by 59 publications

(39 citation statements)

References 33 publications

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“…and also becomes activated in response to environmental stressors to maintain the cellular homeostasis (31,76). The conversion of LC3-I to LC3-II and the formation of autophagosomes are hallmark features of autophagy (58).…”

Section: Discussionmentioning

confidence: 99%

“…cancer and neurological and neurodegenerative disorders, such as Parkinson and Alzheimer disease) (25,27,28). Recent studies have found that several environmental toxicants, such as arsenic (29), cadmium, chromium (30,31), dibenzofuran (32), paraquat (33), and ethanol (34,35), cause alterations in the basal levels of autophagy, leading to cellular toxicity. Autophagy acts as a cardinal process and interconnects several cell survival pathways (viz.…”

Section: Bisphenol-a (Bpa)mentioning

confidence: 99%

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Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

Agarwal

Tiwari

Seth

et al. 2015

Journal of Biological Chemistry

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Background:The effects of xenoestrogen bisphenol-A on autophagy, and association with oxidative stress and apoptosis are still elusive. Results: Transient activation of autophagy protects against bisphenol-A-induced neurodegeneration via AMPK activation and mTOR down-regulation. Conclusion: Autophagy induction against bisphenol-A is an early cell's tolerance response. Significance: Autophagy provides an imperative biological marker for evaluation of neurotoxicity by xenoestrogen.

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Section: Discussionmentioning

confidence: 99%

Section: Bisphenol-a (Bpa)mentioning

confidence: 99%

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

Agarwal

Tiwari

Seth

et al. 2015

Journal of Biological Chemistry

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“…[7][8][9] Furthermore, autophagy was identified as a biomarker of heavy metal toxicity in human stem cells. 10 However, at present, there are few studies on the role of autophagy during development and on the putative protective function that it has in embryos exposed to stress.…”

Section: Introductionmentioning

confidence: 99%

Sea urchin embryos as a model system for studying autophagy induced by cadmium stress

Chiarelli¹,

Agnello²,

Roccheri³

2011

Autophagy

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In this paper we utilized different techniques to detect autophagy in sea urchin embryos. Using neutral red (NR) and acridine orange (AO) vital staining, we found that embryos exposed to Cd display massive punctiform spots in the cytoplasm, indicative of acidic vesicular organelles (AVOs). These results have been confirmed using bafilomycin A 1 , a known inhibitor of this process. Furthermore these data were validated through both protein gel blotting and immunofluorescence in situ analysis of LC3-II, a specific marker of autophagy.We found that in P. lividus embryos autophagic processes occur in lesser amounts during physiological development and in greater amounts after Cd exposure.

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“…Cd has a critical role throughout evolution of biota that is naturally exposed to fluctuating levels of these toxicants [35]. The higher chronic exposure occurs in mines and industrial workers such as smelting, battery manufacturing and pigment production or residents of cadmium-polluted areas close to these industries.…”

Section: Discussionmentioning

confidence: 99%

Autophagy Plays a Cytoprotective Role During Cadmium-Induced Oxidative Damage in Primary Neuronal Cultures

Wang

Song

et al. 2015

Biol Trace Elem Res

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Cadmium (Cd) induces significant oxidative damage in cells. Recently, it was reported that autophagy could be induced by Cd in neurons. However, little is known about the role of reactive oxygen species (ROS) during Cd-induced autophagy. In our study, we examined the cross-talk between ROS and autophagy by using N-acetyl cysteine (NAC, an antioxidant) and chloroquine (CQ, a pharmacological inhibitor of autophagy) in a primary rat neuronal cell cultures. We observed accumulation of acidic vesicular organelles and the increased expression of endogenous protein light chain 3 (LC3) in Cd-treated neurons, revealing that Cd induced a high level of autophagy. Moreover, increased levels of ROS were observed in neurons treated with Cd, showing that ROS accumulation was closely associated with neuron's exposure to Cd. Furthermore, we found that autophagy was inhibited by using CQ and/or NAC with further aggravation of mitochondrial damage, lactate dehydrogenase (LDH) leakage and hypoploid apoptotic cell number in Cd-treated neurons. These results proved that autophagy has a cytoprotective role during Cd-induced toxicity in neurons, and it can prevent the oxidative damage. These findings may enable the development of novel therapeutic strategies for neurological diseases.

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Autophagy as an ultrastructural marker of heavy metal toxicity in human cord blood hematopoietic stem cells

Cited by 59 publications

References 33 publications

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

Activation of Autophagic Flux against Xenoestrogen Bisphenol-A-induced Hippocampal Neurodegeneration via AMP kinase (AMPK)/Mammalian Target of Rapamycin (mTOR) Pathways

Sea urchin embryos as a model system for studying autophagy induced by cadmium stress

Autophagy Plays a Cytoprotective Role During Cadmium-Induced Oxidative Damage in Primary Neuronal Cultures

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