Effects of N-acetyl-l-cysteine,in vivo, against pathological changes induced by malathion

Abstract

Malathion toxicity has been related to the inhibition of acetylcholinesterase, induction of oxidative stress, liver damage and impairment of kidney function as well as hematotoxicity. N-acetyl-l-cysteine (NAC) has been shown to possess curative effects in experimental and clinical investigations. The present study was designed to evaluate the protective effect of NAC against toxic consequences of malathion exposure in Wistar rats. Malathion was given daily to rats via oral gavage and NAC in drinking water during seven days. When malathion-treated rats were compared with control, a leukocytosis and reduced hemoglobin (HGB) content were detected. Furthermore, malathion produced a significant increase in liver enzymes such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, lactate dehydrogenase and creatinine kinase. In addition, a decrease in acid phosphatase activity, protein and globulin levels were observed in malathion-treated rats compared with control. Moreover, analyses of the mineral status showed a disturbance in calcium, magnesium, phosphore and iron contents of the malathion-treated rats. Interestingly, NAC showed therapeutic effects against malathion toxicity. Indeed, HGB content and all liver enzymes were restored to normal values. Finally, the use of NAC as therapeutic agent for only seven days during malathion exposure showed interesting results on tissues damages.

Corticosterone and pyridostigmine/DEET exposure attenuate peripheral cytokine expression: Supporting a dominant role for neuroinflammation in a mouse model of Gulf War Illness

“…This observation suggests that the more brain-exclusive inflammatory priming we find in our GWI model may be specific to DFP, and other OP exposures. However, OP compounds have been identified to cause liver damage and associated inflammation (Mostafalou et al, 2012; Lasram et al, 2014; Ezzi et al, 2016), supported by the observed increases in IL-6, IL-1b, LIF, and OSM mRNA in the liver and IL-6 and KC levels in the serum, though these responses were generally suppressed by CORT. Our hypothesis is that exposure to DFP directly instigates neuroinflammation that can be primed by CORT, as we have observed no indicators of neuronal damage in these mice (O’Callaghan et al, 2015), while the peripheral cytokine responses are the result of liver damage-induced inflammation that is non-responsive to prior CORT exposure (Fig.…”

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

“…However, liver GSH levels in the current study were increased by NAC administration because of facilitating GSH biosynthesis. Number of researchers suggested that NAC is effective as a chelating agent in reducing the toxicity of pesticide when it administrated on intoxicated animals (Borgstrom et al 1986;Zimet 1988;Lasram et al 2014b). …”

Occupational exposure to pesticides and hematological alterations: A survey of farm residents in the South of Brazil

“…For instance, insecticide cypermethrin (synthetic pyrethroid) inhibited erythroid and granulocyte-macrophage progenitors in vitro 31 , while low doses of the OP mevinphos caused destruction of progenitors in human and rat hematopoietic progenitor cells 32 . There is also experimental evidence that insecticides malathion (OP) and carbaryl (carbamate) may induce anemia, immunosuppression, and altered number of leukocytes and platelets in vivo 33,34 . It is noteworthy to mention that previous studies have reported elevated risks for lymphatic and hematopoietic neoplasms, including chronic lymphoid leukemia, Hodgkin and non-Hodgkin lymphoma, and multiple myeloma, among farmers 35,36 and workers occupationally exposed to OP insecticides 37 .…”