Association of inflammatory response and oxidative injury in the pathogenesis of liver steatosis and insulin resistance following subchronic exposure to malathion in rats

Lasram, Mohamed Montassar; Dhouib, Ines Bini; Bouzid, K; Lamine, Aicha Jrad; Annabi, Alya; Belhadjhmida, Nadia; Ahmed, Malika Ben; Fazâa, Saloua El; Abdelmoula, J.; Gharbi, N.

doi:10.1016/j.etap.2014.08.007

Cited by 43 publications

(22 citation statements)

References 69 publications

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“…Carbosulfan induces spleen toxicity in part by increasing of free radical production (El-Bini Dhouib et al 2014). Lipid peroxidation is known to be one of the molecular mechanisms for cell injury in pesticide poisoning and is associated with a decrease in cellular antioxidants such as superoxide dismutase and catalase (Kaur and Sandhir 2006;Lasram et al 2014a). Hepatic catalase activity was found to be increased in this study.…”

Section: Discussionmentioning

confidence: 99%

“…Anti-cholinesterase pesticides mainly include organophosphates such as malathion as well as carbamates such as carbofuran and carbosulfan. The acute toxicity of these pesticides has been well documented (de Silva et al 1992;Gupta 1994;Smulders et al 2003;Raheja and Gill 2007;Lasram et al 2009Lasram et al , 2014a. Liver, which is the main organ responsible for metabolism, is a common target of pesticide toxicity (Celik et al 2009).…”

Section: Carbosulfan-induced Oxidative Damage Following Subchronic Exmentioning

confidence: 99%

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Carbosulfan-induced oxidative damage following subchronic exposure and the protective effects of N-acetylcysteine in rats

Dhouib¹,

Annabi²,

Jrad³

et al. 2015

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Abstract. Carbosulfan (CB)-induced oxidative stress leads to the inevitable accumulation of free radicals and eventual alteration of antioxidant enzymes in various biological systems. The present study is designed to investigate the preventive effect of N-acetylcysteine (NAC) on carbosulfaninduced hepatic and renal dysfunction in rats. Rats exposed to CB and NAC were examined for toxicity by assessing various biochemical alteration and stress markers including in liver and kidney. Significant increases of blood alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT), creatinine and urea were detected in CB-treated rats. In addition, the levels of antioxidative enzymes such as catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH) also were assessed. According to the results, rats exposed to carbosulfan showed a significant increase in the accumulation of stress markers and an alteration in the antioxidative enzymes activity, when compared to their respective controls. Interestingly, administration of NAC to CB-treated rats attenuates the toxicity of this compound, objectified by biochemical and oxidative improvement of liver and kidney. Thus, the present study reports for the first time that NAC could be a promising therapeutic agent against CB-induced oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Section: Carbosulfan-induced Oxidative Damage Following Subchronic Exmentioning

confidence: 99%

Carbosulfan-induced oxidative damage following subchronic exposure and the protective effects of N-acetylcysteine in rats

Dhouib¹,

Annabi²,

Jrad³

et al. 2015

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“…Conversely, this putative association has been examined only in a few experimental studies in rodent models of insulin resistance. Thus, a recent study revealed that the increment of immune cells may be a consequence of the increased expression of cytokines, including IL-1, IL-6 and IFN-γ in the liver of rats exposed to malathion ( 82 ). Moreover, Zhang et al demonstrated enhanced levels of malondialdehyde, TNF-α and IL-6 in the muscles of rats exposed to omethoate, a commonly used insecticide in developing countries ( 83 ).…”

Section: Diabetesmentioning

confidence: 99%

Occupational and environmental exposure to pesticides and cytokine pathways in chronic diseases (Review)

Gangemi

Gofita

Costa

et al. 2016

International Journal of Molecular Medicine

149

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Pesticides can exert numerous effects on human health as a consequence of both environmental and occupational exposures. The available knowledge base suggests that exposure to pesticides may result in detrimental reproductive changes, neurological dysfunction and several chronic disorders, which are defined by slow evolution and long-term duration. Moreover, an ever increasing amount of data have identified an association between exposure to pesticides and the harmful effects on the immune system. The real impact of alterations in humoral cytokine levels on human health, in particular in the case of chronic diseases, is still unclear. To date, studies have suggested that although exposure to pesticides can affect the immune system functionally, the development of immune disorders depends on the dose and duration of exposure to pesticides. However, many of the respective studies exhibit limitations, such as a lack of information on exposure levels, differences in the pesticide administration procedures, difficulty in characterizing a prognostic significance to the weak modifications often observed and the interpretation of obtained results. The main challenge is not just to understand the role of individual pesticides and their combinations, but also to determine the manner and the duration of exposure, as the toxic effects on the immune system cannot be separated from these considerations. There is a clear need for more well-designed and standardized epidemiological and experimental studies to recognize the exact association between exposure levels and toxic effects and to identify useful biomarkers of exposure. This review focuses on and critically discusses the immunotoxicity of pesticides and the impact of cytokine levels on health, focusing on the development of several chronic diseases.

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“…Atessahin et al (2005) have reported that cypermetrin leads to lipid peroxidation in brain, kidney, and blood. Lasram et al (2014) showed that lipid peroxidation is increased in the liver of malathion-exposed rats. The significant increase of MDA, the index of lipid peroxidation, in HPA tissues following IMI treatment is an important evidence of lipid peroxidation in the present study.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Imidacloprid-Induced Alteration of Hypothalamic-Pituitary-Adrenal (HPA) Axis after Subchronic Exposure in Male Rats

Annabi¹,

Dhouib²,

Dkhili³

et al. 2015

Recent Advances in Biology and Medicine

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Imidacloprid (IMI) is known to target the nicotinic acetylcholine receptors (nAChRs) in insects, and potentially in mammals. However, IMI toxicity on mammalian tissues has not been adequately evaluated. The aim of the present study was to examine whether IMI induced functional impairment in hypthalamic-pituitary-adrenal (HPA) axis tissues. An oral exposure of 40 mg IMI/kg for 28 days in male rats caused a significant increase in malondialdehyde (MDA) level. The antioxidant catalase, superoxide dismutase, and glutathione S-transferase showed various alterations following administration, but a significantly depleted thiol (SH) groups was only recorded in hypothalamic tissues. The increase in the relative weight of adrenal glands and the increased adrenal cholesterol and plasma adrenocorticotropic hormone (ACTH) levels are indicative of general adaptation syndrome. The hypothalamic and pituitary acetylcholinesterase activity and calcium level were significantly increased, highlighting the alteration of cholinergic transmission. In conclusion, the findings obtained show that chronic exposure to IMI may alter biochemical processes of HPA axis.

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Association of inflammatory response and oxidative injury in the pathogenesis of liver steatosis and insulin resistance following subchronic exposure to malathion in rats

Cited by 43 publications

References 69 publications

Carbosulfan-induced oxidative damage following subchronic exposure and the protective effects of N-acetylcysteine in rats

Carbosulfan-induced oxidative damage following subchronic exposure and the protective effects of N-acetylcysteine in rats

Occupational and environmental exposure to pesticides and cytokine pathways in chronic diseases (Review)

Mechanisms of Imidacloprid-Induced Alteration of Hypothalamic-Pituitary-Adrenal (HPA) Axis after Subchronic Exposure in Male Rats

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