Protective effect of N-acetyl-L-cysteine against maneb induced oxidative and apoptotic injury in Chinese hamster V79 cells

Grosicka-Maciąg, Emilia; Kurpios-Piec, Dagmara; Szumiło, Maria; Grzela, Tomasz; Rahden-Staroń, Iwonna

doi:10.1016/j.fct.2011.01.009

Cited by 29 publications

(13 citation statements)

References 31 publications

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“…In this study, the observed decrease in GSH could be explained by disruption of the GSH production by free radicals. This is in agreement with a previous study by Grosicka-Maciąg et al (2011), who have shown that MB decreased GSH and increased GSSG levels in Chinese hamster V79 cells. Similar results were also observed for type PC 12 dopaminergic rat cells exposed to MB (Barlow et al 2005).…”

Section: Discussionsupporting

confidence: 95%

“…Previous studies of Bertini et al (2000) have shown that MB modifies the activity of a variety of P450 isoenzymes, leading to a greater production of ROS and hepatotoxicity in rabbit. Likewise, Grosicka-Maciąg et al (2011) have demonstrated in V79 hamsters cells that MB generated ROS via carrier inhibition of the electrons in the mitochondrial chain or inhibition of proteosomal activity. In this study, oxidative stress in the liver of experimental mice was also confirmed by a novel marker, AOPP, which reflected an excess of free radical generation and protein oxidative damage.…”

Section: Discussionmentioning

confidence: 96%

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Maneb disturbs expression of superoxide dismutase and glutathione peroxidase, increases reactive oxygen species production, and induces genotoxicity in liver of adult mice

Amara

Saad

Hamdaoui

et al. 2015

Environ Sci Pollut Res

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Maneb (MB), a fungicide largely used in agriculture throughout the world including Tunisia, protects many vegetables, fruits and field crops against a wide spectrum of fungal diseases. However there is a lack of informations regarding the risks arising from MB exposure on non target organisms, especially mammals. The aim of this study was to investigate the morphological, biochemical and molecular aspects of liver injury after exposure of mice to MB. Four doses of MB corresponding to 1/8 (group D1), 1/6 (group D2), 1/4 (group D3), and 1/2 (group D4) of lethal dose (DL50 = 1500 mg/kg body weight) were administered to adult mice. Oxidative stress parameters were also objectified by molecular and histological endpoints in the liver. Maneb caused hepatotoxicity as characterized by the significant increase in the levels of malondialdehyde and protein oxidation marker, advanced oxidation protein products (AOPP). The activities of catalase, glutathione peroxidase, superoxide dismutase and the levels of glutathione decreased significantly in all treated mice, while vitamin C levels decreased only in group D4. We also noted a significant decrease in gene expression of superoxide dismutase and glutathione peroxidase enzymes. Maneb caused nucleic acids degradation testifying its genotoxicity. Yet, biochemical markers in plasma showed a decrease in total protein and an increase in aspartate, alanine amino transferases and bilirubin levels in all treatment groups. Moreover, plasma levels of cholesterol, triglycerides and low density lipoprotein-cholesterol significantly increased, while those of high density lipoprotein-cholesterol decreased. These biochemical alterations were correlated with significantly histological changes. Our data showed, for the first time, that intraperitoneal injection of very high non environmentally relevant MB concentrations to adult mice resulted in oxidative stress leading to hepatotoxicity and the impairment of defense systems, confirming the pro-oxidant and genotoxic effects of this fungicide.

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Section: Discussionsupporting

confidence: 95%

Section: Discussionmentioning

confidence: 96%

Maneb disturbs expression of superoxide dismutase and glutathione peroxidase, increases reactive oxygen species production, and induces genotoxicity in liver of adult mice

Amara

Saad

Hamdaoui

et al. 2015

Environ Sci Pollut Res

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“…Since NAC did not increase total liver GSH, but reduced the level of oxidized GSH in PCB 126 exposed and control animals (Lai et al 2012), and serum TBARS were significantly lower in the NAC controls compared to normal controls. Similar protective effects of NAC were reported in other animal and cell culture studies (Grosicka-Maciag et al 2011; Sciuto et al 1995; Vendemiale et al 2001). Quercetin, another dietary antioxidant supplement, also preserved PON1 activity, which was attributed to either prevention of GSH depletion (Varatharajalu et al 2009) or induction of PON1 gene expression (Aviram 2006).…”

Section: Discussionsupporting

confidence: 89%

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Shen

Wang

et al. 2013

Environ Sci Pollut Res

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The environmental pollutants polychlorinated biphenyls (PCBs), especially dioxin-like PCBs, cause oxidative stress and associated toxic effects, including cancer and possibly atherosclerosis. We previously reported that PCB 126, the most potent dioxin-like PCB congener, decreases antioxidants such as hepatic selenium (Se), selenium-dependent glutathione peroxidase and glutathione (GSH), but also increases levels of the anti-atherosclerosis enzyme paraoxonase 1 (PON1) in liver and serum. To probe the interconnection of these three antioxidant systems, Se, GSH, and PON1, we examined the influence of varying levels of dietary Se and N-acetylcysteine (NAC), a scavenger of reactive oxygen species (ROS) and precursor for GSH synthesis, on PON1 in the absence and presence of PCB 126 exposure. Male Sprague Dawley rats, fed diets with differing Se levels (0.02, 0.2, or 2 ppm) or NAC (1%), were treated with a single intraperitoneal injection of corn oil or various doses of PCB 126 and euthanized 2 weeks later. PCB126 significantly increased liver PON1 mRNA, protein level and activity and serum PON1 activity in all dietary groups, but did not consistently increase thiobarbituric acid levels (TBARS), an indicator for lipid oxidation and oxidative stress, in liver or serum. Inadequate (high or low) dietary Se decreased baseline and PCB 126-induced aryl hydrocarbon receptor expression but further increased PCB 126-induced cytochrome P450 1A1 expression, the enzyme believed to be the cause for PCB 126-induced oxidative stress. In addition, a significant inverse relationship was observed between dietary Se levels and PON1 mRNA and PON1 activity, but also with TBARS levels in the liver, suggesting significant antioxidant protection from dietary Se. NAC lowered serum baseline TBARS levels in the controls and increased serum PON1 activity but lowered liver PON1 activities in animals treated with 1 μmol/kg PCB 126, suggesting antioxidant activity by NAC primarily in serum. These results also show an unexpectedly predominantly inverse relationship between Se or NAC and PON1 during normal and PCB 126 exposure conditions. These interactions should to be further explored in the development of dietary protection regimens.

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“…Previous data show that NAC pretreatment can protect against MB-induced injury in Chinese hamster V79 cells, indicating that increased cellular thiols can protect or even prevent toxicity associated with an acute MB exposure [17]. With this in mind, the present data indicate that relatively slow, reversible binding of MB with protein thiols could trap MB in cells.…”

Section: Discussionsupporting

confidence: 57%

Thiol-reactivity of the fungicide maneb

Roede

Jones

2014

Redox Biology

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Maneb (MB) is a manganese-containing ethylene bis-dithiocarbamate fungicide that is implicated as an environmental risk factor for Parkinson's disease, especially in combination with paraquat (PQ). Dithiocarbamates inhibit aldehyde dehydrogenases, but the relationship of this to the combined toxicity of MB + PQ is unclear because PQ is an oxidant and MB activates Nrf2 and increases cellular GSH without apparent oxidative stress. The present research investigated the direct reactivity of MB with protein thiols using recombinant thioredoxin-1 (Trx1) as a model protein. The results show that MB causes stoichiometric loss of protein thiols, reversibly dimerizes the protein and inhibits its enzymatic activity. MB reacted at similar rates with low-molecular weight, thiol-containing chemicals. Together, the data suggest that MB can potentiate neurotoxicity of multiple agents by disrupting protein thiol functions in a manner analogous to that caused by oxidative stress, but without GSH depletion.

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Protective effect of N-acetyl-L-cysteine against maneb induced oxidative and apoptotic injury in Chinese hamster V79 cells

Cited by 29 publications

References 31 publications

Maneb disturbs expression of superoxide dismutase and glutathione peroxidase, increases reactive oxygen species production, and induces genotoxicity in liver of adult mice

Maneb disturbs expression of superoxide dismutase and glutathione peroxidase, increases reactive oxygen species production, and induces genotoxicity in liver of adult mice

Dietary antioxidants (selenium and N-acetylcysteine) modulate paraoxonase 1 (PON1) in PCB 126-exposed rats

Thiol-reactivity of the fungicide maneb

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