Oxidative stress-induced autophagy: Role in pulmonary toxicity

Malaviya, Rama; Laskin, Jeffrey D.; Laskin, Debra L.

doi:10.1016/j.taap.2013.12.022

Cited by 28 publications

(27 citation statements)

References 93 publications

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“…In the lungs, hypoxia can induce oxidative stress and inflammation that can cause bronchial vasoconstriction, pulmonary oedema, vascular remodelling and pulmonary hypertension (Araneda and Tuesta 2012). In addition, oxidative stress in the lungs may induce autophagy, which is a catabolic process that regulates turnover of proteins and eliminates damaged organelles and protein aggregates (Malaviya et al 2014). Furthermore, hypoxia may cause epigenetic effects due to dysregulation of histone methylation (Chervona and Costa 2012).…”

Section: Genotoxicitymentioning

confidence: 99%

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

2016

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In 2010, the World Health Organization (WHO) established an indoor air quality guideline for short- and long-term exposures to formaldehyde (FA) of 0.1 mg/m3 (0.08 ppm) for all 30-min periods at lifelong exposure. This guideline was supported by studies from 2010 to 2013. Since 2013, new key studies have been published and key cancer cohorts have been updated, which we have evaluated and compared with the WHO guideline. FA is genotoxic, causing DNA adduct formation, and has a clastogenic effect; exposure–response relationships were nonlinear. Relevant genetic polymorphisms were not identified. Normal indoor air FA concentrations do not pass beyond the respiratory epithelium, and therefore FA’s direct effects are limited to portal-of-entry effects. However, systemic effects have been observed in rats and mice, which may be due to secondary effects as airway inflammation and (sensory) irritation of eyes and the upper airways, which inter alia decreases respiratory ventilation. Both secondary effects are prevented at the guideline level. Nasopharyngeal cancer and leukaemia were observed inconsistently among studies; new updates of the US National Cancer Institute (NCI) cohort confirmed that the relative risk was not increased with mean FA exposures below 1 ppm and peak exposures below 4 ppm. Hodgkin’s lymphoma, not observed in the other studies reviewed and not considered FA dependent, was increased in the NCI cohort at a mean concentration ≥0.6 mg/m3 and at peak exposures ≥2.5 mg/m3; both levels are above the WHO guideline. Overall, the credibility of the WHO guideline has not been challenged by new studies.

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Section: Genotoxicitymentioning

confidence: 99%

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

2016

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“…Because of its functions: elimination, salvage, and repair, autophagy is regarded as a cell survival mechanism in general (Levine and Klionsky, 2004;Rodrigues et al, 2009). When oxidative stress occurs, autophagy can eliminate those oxidized proteins and damaged mitochondria, for example, in cardiac myocytes during ischemia/reperfusion (Hariharan et al, 2011) and in pulmonary tissue (Malaviya et al, 2014). Wang et al proposed that autophagy is closely related to acrosome biogenesis during spermatogenesis in mice (Wang et al, 2014b).…”

Section: Introductionmentioning

confidence: 99%

Bisphenol a induces autophagy and apoptosis concurrently involving the Akt/mTOR pathway in testes of pubertal SD rats

Quan

Wang

Duan

et al. 2016

Environmental Toxicology

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Bisphenol A (BPA), a typical endocrine disrupting chemical (EDC), has been proven to cause male reproductive toxicity. However, the precise mechanisms of this effect are still unclear. Puberty is a crucial period of reproductive development, and adolescents are more susceptible to xenobiotics. This research was designed to explore the mechanism of BPA toxicity on pubertal male reproduction. Rats were exposed to 0, 2, 10, 50 mg kg bw BPA, then the levels of sex hormones, oxidative stress, and semen quality were detected. HE staining, TUNEL assay and transmission electron microscopy were used to investigate the morphological changes, apoptosis, and autophagy in testes, respectively. Expressions of relevant genes and proteins were measured by RT-PCR, western blotting, and immunohistochemical staining. The results indicated that BPA exposure led to oxidative stress and endocrine disorders in pubertal male SD rats, caused apoptosis and autophagy in testes, and then damaged spermatogenesis ultimately. The Akt pathway was activated and the mTOR pathway was inhibited in the process. Taken together, BPA induced apoptosis and autophagy concurrently in pubertal testes, and this added a new layer to our understanding on male reproductive toxicity of BPA. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1977-1989, 2017.

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“…A large number of xenobiotics (pesticides, herbicides) and chemicals (alcohol) also produce ROS as a by‐product of their metabolism in cells [Siriwardena, ]. Air pollutants such as car exhaust, cigarette smoke, industrial contaminants, and engineered NM derivatives constitute major environmental sources of ROS‐producing compounds that come in contact with the organism either by direct interaction with skin, or more importantly, following inhalation into the lungs [Bono et al, ; Esposito et al, ; Johnston et al, ; Liu et al, ; Malaviya et al, ]. Finally, ROS are also generated by phagocytes (mainly in the phagocytosis process) within the phagosomal membrane for efficient killing of foreign antigens [West et al, ].…”

Section: Introductionmentioning

confidence: 99%

The role of intracellular redox imbalance in nanomaterial induced cellular damage and genotoxicity: A review

Kermanizadeh

Chauché

Brown

et al. 2014

Environ and Mol Mutagen

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The terms oxidative stress, free radical generation, and intracellular antioxidant protection have become part of everyday nanotoxicology terminology. In recent years, an ever increasing number of in vitro and in vivo studies have implicated disruptions to the redox balance and oxidative stress as one of the main contributors to nanomaterial (NM) induced adverse effects. One of the most important and widely investigated of these effects is genotoxicity. In general, systems that defend an organism against oxidative damage to DNA are very complex and include prevention of reactive oxygen species (ROS) production, neutralizing ROS (scavengers), enzymatic nucleotide pool sanitation, and DNA repair. This review discusses the importance of the maintenance of the redox balance in this context before examining studies that have investigated engineered NM induced redox imbalance and genotoxicity. Furthermore, we identify data gaps, and highlight a number of issues that exist with the methodologies that are routinely utilized to investigate intracellular ROS production or anti-oxidant depletion. We conclude that for a large number of engineered NM types changes in the redox balance toward oxidative stress are normally associated with DNA damage.

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Oxidative stress-induced autophagy: Role in pulmonary toxicity

Cited by 28 publications

References 93 publications

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

Re-evaluation of the WHO (2010) formaldehyde indoor air quality guideline for cancer risk assessment

Bisphenol a induces autophagy and apoptosis concurrently involving the Akt/mTOR pathway in testes of pubertal SD rats

The role of intracellular redox imbalance in nanomaterial induced cellular damage and genotoxicity: A review

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