Hormetic effects of noncoplanar PCB exposed to human lung fibroblast cells (HELF) and possible role of oxidative stress

Hashmi, Muhammad Zaffar; Khan, Kiran Yasmin; Hu, Jinxing; Naveedullah,; Su, Xiaomei; Abbas, Ghulam; Yu, Chunna; Shen, Chaofeng

doi:10.1002/tox.22008

Cited by 14 publications

(14 citation statements)

References 37 publications

(48 reference statements)

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“…This was in line with the previous reports that MAPK activation has been implicated by ROS-mediated oxidative stress 55 and induced cell death in PCBs exposed rat hepatocyte cell, 56 mussel hemocytes, 57 human MDA-MB-231 (MDA), 58 human kidney cells (HK2), 52 MCF-7 breast cancer cells, 59 and HELF cells. 34 Interestingly, this result is supporting our hypothesis that MAPK cascade is involved in the adaptive response of low doses and inhibitory response of high doses of PCBs on HeLa cells which commonly displays hormesis.…”

Section: Discussionsupporting

confidence: 79%

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Biphasic Dose–Response Induced by PCB150 and PCB180 in HeLa Cells and Potential Molecular Mechanisms

et al. 2020

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The polychlorinated biphenyls (PCBs) are persistent and their dose-dependent toxicities studies are not well-established. In this study, cytotoxic and genotoxic effects of PCB150 and PCB180 in HeLa cells were studied. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay indicated that the cell proliferation was stimulated at low doses (10−3 and 10−2 µg/mL for 12, 24, 48, and 72 hours) and inhibited at high doses (10 and 15 µg/mL for 24, 48, and 72 hours) for both PCBs. Increase in reactive oxygen species formation was observed in the HeLa cells in a time- and dose-dependent manner. Malondialdehyde and superoxide dismutase showed increased levels at high concentrations of PCBs over the time. Glutathione peroxidase expression was downregulated after PCBs exposure, suggested that both PCB congeners may attributable to cytotoxicity. Comet assay elicited a significant increase in genotoxicity at high concentrations of PCBs as compared to low concentrations indicating genotoxic effects. PCB150 and PCB180 showed decrease in the activity of extracellular signal–regulated kinase 1/2 and c-Jun N-terminal kinase at high concentrations after 12 and 48 hours. These findings may contribute to understanding the mechanism of PCBs-induced toxicity, thereby improving the risk assessment of toxic compounds in humans.

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Section: Discussionsupporting

confidence: 79%

“…Taken together, our study is in accordance with previous studies that highlighted predominantly expressed ROS levels abolishes GSH which inevitably leads to compromised DNA function and integrity. 34…”

Section: Discussionmentioning

confidence: 99%

Biphasic Dose–Response Induced by PCB150 and PCB180 in HeLa Cells and Potential Molecular Mechanisms

et al. 2020

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“…Reports in the literature show that other molecules besides SIH iron chelators can induce oxidative hormesis via Nrf2 in mammalian cells, suggesting a general antioxidant mechanism. For example, oxidative hormesis effects induced by Nrf2 were observed in murine fibrosarcoma L929 cells exposed to H 2 O 2 [35], in human endothelial EA.hy926 cells exposed to docosahexaenoic acid [36], and in human lung fibroblast HELF cells exposed to polychlorinated biphenyls [37]. …”

Section: Discussionmentioning

confidence: 99%

Prooxidant and antioxidant properties of salicylaldehyde isonicotinoyl hydrazone iron chelators in HepG2 cells

Andrés

Commissariat

Dunn

et al. 2015

Biochimica et Biophysica Acta (BBA) - General Subjects

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Background Salicylaldehyde isonicotinoyl hydrazone (SIH) is an iron chelator of the aroylhydrazone class that displays antioxidant or prooxidant effects in different mammalian cell lines. Because the liver is the major site of iron storage, elucidating the effect of SIH on hepatic oxidative metabolism is critical for designing effective hepatic antioxidant therapies. Methods Hepatocyte-like HepG2 cells were exposed to SIH or to analogs showing greater stability, such as N′-[1-(2-Hydroxyphenyl)ethyliden]isonicotinoyl hydrazide (HAPI), or devoid of iron chelating properties, such as benzaldehyde isonicotinoyl hydrazone (BIH), and toxicity, oxidative stress and antioxidant (glutathione) metabolism were evaluated. Results Autoxidation of Fe2+ in vitro increased in the presence of SIH or HAPI (but not BIH), an effect partially blocked by Fe2+ chelation. Incubation of HepG2 cells with SIH or HAPI (but not BIH) was non-toxic and increased reactive oxygen species (ROS) levels, activated the transcription factor Nrf2, induced the catalytic subunit of γ-glutamate cysteine ligase (Gclc), and increased glutathione concentration. Fe2+ chelation decreased ROS and inhibited Nrf2 activation, and Nrf2 knock-down inhibited the induction of Gclc in the presence of HAPI. Inhibition of γ-glutamate cysteine ligase enzymatic activity inhibited the increase in glutathione caused by HAPI, and increased oxidative stress. Conclusions SIH iron chelators display both prooxidant (increasing the autoxidation rate of Fe2+) and antioxidant (activating Nrf2 signaling) effects. General significance Activation by SIH iron chelators of a hormetic antioxidant response contributes to its antioxidant properties and modulates the anti- and pro-oxidant balance.

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“…In the last years many treatments to induce the hormetic response in order to counteract oxidative damage have been described (Hine and Mitchell 2012;Kubicova et al 2013;Hashmi et al 2014), however few of them have described in detail the molecular mechanisms during OCH.…”

Section: Parallel Mechanisms During Hormetic Oxidative Responsementioning

confidence: 99%

New considerations on hormetic response against oxidative stress

Luna–López

González-Puertos

López‐Díazguerrero

et al. 2014

J. Cell Commun. Signal.

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In order to survive living organisms have developed multiple mechanisms to deal with tough environmental conditions. Hormesis is defined as a process in which exposure to a low dose of a chemical agent or environmental factor that is damaging at higher doses induces an adaptive beneficial effect on the cell or organism. In this paper, we examine several ideas that might be taken into consideration before using hormesis as a therapeutic tool to improve health and life span, and hopefully will open the discussion for new and interesting debates regard hormesis. The first one is to understand that the same stressor or inductor can activate different pathways in a parallel or dual response, which might lead to diverse outcomes. Another idea is related to the mechanisms involved in activating Nrf2, which might be different and have diverse hormetic effects.Last, we discuss mild oxidative stress in association to lowgrade chronic inflammation as a stimulating avenue to be explored and the unexpected effects proposed by the obesity paradox theory. All the previous might help to clarify the reasons why centenarians are able to reach the extreme limits of human life span, which could probably be related to the way they deal with homeostasis maintenance, providing an opportunity for hormesis to intervene significantly.

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Hormetic effects of noncoplanar PCB exposed to human lung fibroblast cells (HELF) and possible role of oxidative stress

Cited by 14 publications

References 37 publications

Biphasic Dose–Response Induced by PCB150 and PCB180 in HeLa Cells and Potential Molecular Mechanisms

Biphasic Dose–Response Induced by PCB150 and PCB180 in HeLa Cells and Potential Molecular Mechanisms

Prooxidant and antioxidant properties of salicylaldehyde isonicotinoyl hydrazone iron chelators in HepG2 cells

New considerations on hormetic response against oxidative stress

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