New considerations on hormetic response against oxidative stress

Luna–López, Armando; González-Puertos, Viridiana Yazmín; López‐Díazguerrero, Norma Edith; Königsberg, Mina

doi:10.1007/s12079-014-0248-4

Cited by 41 publications

(29 citation statements)

References 95 publications

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“…Oxidative hormesis is defined as a process in which exposure to a low dose of an oxidant induces an adaptive antioxidant protective response [34]. While SIH is usually classified as a preventive antioxidant, our results suggest that SIH iron chelators can also display antioxidant effects via an oxidative hormesis effect mediated by Nrf2 activation.…”

Section: Discussionmentioning

confidence: 64%

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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Section: Discussionmentioning

confidence: 64%

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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“…EDCs are capable of mediating changes in methylation patterns and regulate epigenetic encoding in cells, and epigenetic program control by such compounds are now well documented [67–70]. Oxidative stresses are now also considered [31, 71]. A number of genes, viz.…”

Section: Endocrine Disrupting Chemicals (Pcbs Exposures) and Developmmentioning

confidence: 99%

Biomarkers Linking PCB Exposure and Obesity.

Ghosh¹,

Murínová²,

Trnovec³

et al. 2014

CPB

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Recently the prevalence of obesity has increased dramatically across much of the world. Obesity, as a complex, multifactorial disease, and its health consequences probably result from the interplay of environmental, genetic, and behavioral factors. Several lines of evidence support the theory that obesity is programmed during early development and that environmental exposures can play a key role. We therefore hypothesize that the current epidemic might associated with the influence of chemical exposures upon genetically controlled developmental pathways, leading to metabolic disorders. Some environmental chemicals, such as PCBs and pesticide residues, are widespread in food, drinking water, soil, and they exert multiple effects including estrogenic on cellular processes; some have been shown to affect the development of obesity, insulin resistance, type 2 diabetes, and metabolic syndrome. To bring these lines of evidence together and address an important health problem, this narrative review has been primarily designed to address PCBs exposures that have linked with human disease, obesity in particular, and to assess the effects of PCBs on gene expression in a highly-exposed population. The results strongly suggest that further research into the specific mechanisms of PCBs-associated diseases is warranted.

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“…For example, it has been shown that reactive oxygen species activate the nuclear transcription factor erythroid-derived 2-like 2 (Nrf2), which induces the expression of various antioxidant enzymes, and provide cells effective neutralization and clearance mechanisms of these radicals (Dodson et al, 2015;Jimenez-Osorio et al, 2015;Luna-Lopez et al, 2014;Ma and He, 2012a;Schieber and Chandel, 2014;Wang and Hai, 2011). We have recently shown that α,β-unsaturated reactive 4-hydroxyalkenals also evoke hormetic responses in vascular endothelial cells and pancreatic beta cells exposed to increasing levels of glucose and palmitic acid (Cohen et al, 2011Riahi et al, 2015).…”

Section: Introductionmentioning

confidence: 99%