Lipid peroxidative damage on malathion exposure in rats

Fortunato, Jucélia Jeremias; Agostinho, Fabiano R.; Réus, Gislaine Z.; Petronilho, Fabrícia; Dal‐Pizzol, Felipe; Quevedo, Joao L De

doi:10.1007/bf03033304

Cited by 58 publications

(39 citation statements)

References 35 publications

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“…24) Lipid peroxidation is a major outcome of free-radical-mediated injury, which causes immediate damage to the cell membrane and is related to DNA damage. 25) MDA is a final product of lipid peroxidation, and its level is commonly measured as an indication of lipid peroxidation levels in tissues. 26) GSH, the most abundant antioxidant in cells, plays a major role in the defense against oxidative stress-induced cellular injury and is essential for the maintenance of the intracellular redox balance.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Manassantin A against Ethanol-Induced Gastric Injury in Rats

Song

Seo

Kim

et al. 2016

Biological & Pharmaceutical Bulletin

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Manassantin A, a neolignan isolated from Saururus chinensis, is a major phytochemical compound that has various biological activities, including anti-inflammatory, neuroleptic, and human acyl-CoA : cholesterol acyltransferase (ACAT) inhibitory activities. In this study, we investigated the protective effects of manassantin A against ethanol-induced acute gastric injury in rats. Gastric injury was induced by intragastric administration of 5 mL/kg body weight of absolute ethanol to each rat. The positive control group and the manassantin A group were given oral doses of omeprazole (20 mg/kg) or manassantin A (15 mg/kg), respectively, 1 h prior to the administration of absolute ethanol. Our examinations revealed that manassantin A pretreatment reduced ethanol-induced hemorrhage, hyperemia, and epithelial cell loss in the gastric mucosa. Manassantin A pretreatment also attenuated the increased lipid peroxidation associated with ethanolinduced acute gastric lesions, increased the mucosal glutathione (GSH) content, and enhanced the activities of antioxidant enzymes. The levels of pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β were clearly decreased in the manassantin A-pretreated group. In addition, manassantin A pretreatment enhanced the levels of cyclooxygenase (COX)-1, COX-2, and prostaglandin E 2 (PGE 2 ) and reduced the inducible nitric oxide synthase (iNOS) overproduction and nuclear factor kappa B (NF-κB) phosphorylation. Collectively, these results indicate that manassantin A protects the gastric mucosa from ethanol-induced acute gastric injury, and suggest that these protective effects might be associated with COX/ PGE 2 stimulation, inhibition of iNOS production and NF-κB activation, and improvements in the antioxidant and anti-inflammatory status.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Manassantin A against Ethanol-Induced Gastric Injury in Rats

Song

Seo

Kim

et al. 2016

Biological & Pharmaceutical Bulletin

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“…The interference of acute malathion treatment by increasing end products of protein and lipid peroxidation [11,[13][14][15]21], as well as decreasing antioxidant-related enzymes [11,12,15,21], has been pointed out in previous studies. Similar to zinc, repeated low doses of malathion seem to induce an adaptive response in AChE activity in the rat brain [49].…”

Section: Controlmentioning

confidence: 94%

“…Organophosphate has been considered as an important risk factor for depression and correlated to suicide attempts [9] and has been used as a model of depressive-like behaviour in animals [10]. Malathion, a pesticide widely used to fight fleas, lice, mosquitoes and flies, is thought to be one of the main agents leading to human organophosphate intoxication in the Santa Catarina state, Southern Brazil [11].Along with the induction of depressive-like behaviour in animal models of depression [10,12], malathion toxicity causes impairment in the antioxidant defense [11,12], and produces an increase in several markers of oxidative stress in the rat brain, such as lipid peroxidation, protein carbonylation and DNA damage [13][14][15], but gender differences have not yet been studied.The effects of metals have been under investigation for decades and attention is naturally focused on the most toxic metals such as cadmium, nickel, lead, mercury and arsenic [1]. On the other side, zinc has been considered a relatively safe metal [16] owing to its auto-regulatory metabolism [17] and little attention has been paid to its acute toxicity.…”

mentioning

confidence: 99%

“…Along with the induction of depressive-like behaviour in animal models of depression [10,12], malathion toxicity causes impairment in the antioxidant defense [11,12], and produces an increase in several markers of oxidative stress in the rat brain, such as lipid peroxidation, protein carbonylation and DNA damage [13][14][15], but gender differences have not yet been studied.…”

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confidence: 99%

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Gender Effects of Acute Malathion or Zinc Exposure on the Antioxidant Response of Rat Hippocampus and Cerebral Cortex

Maris

Franco

Mitozo³

et al. 2010

Basic Clin Pharma Tox

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Gender is one of the most important factors in mammalian development and response to exogenous agents. Although there is increasing evidence that health effects of toxic xenobiotics differ in prevalence or are manifested differently in male and female, the molecular mechanisms related to these events remain unclear. In order to investigate the possible influence of gender, male and female Wistar rats from the same litter were exposed to zinc chloride (5 mg ⁄ kg, i.p.) or malathion (250 mg ⁄ kg, i.p.) 24 hr prior to the analyses of biochemical parameters related to the cholinergic and glutathione-antioxidant systems in cerebral cortex and hippocampus. After treatments, acetylcholinesterase (AChE) activity was reduced in the hippocampus and cerebral cortex of male and female rats treated with malathion, but the effect was more pronounced in the male group. Glutathione reductase (GR) and c-glutamyl-transpeptidase activities were reduced in the hippocampus of males and females and a gender-specific effect of malathion was seen for glutathione S-transferase (GST), which was decreased only in male hippocampus and cortex, and for male cortical GR. Zinc chloride treatment decreased AChE activity in male and female cerebral cortex, with no obvious effect in the hippocampus. Male-specific antioxidant-related enzyme activity reductions were seen after zinc treatment for cortical GR, GST, glutathione peroxidase and glucose-6-phosphate dehydrogenase; and hippocampal GR. These results clearly demonstrate a greater detrimental effect on antioxidant-related enzyme activities in male hippocampus and cerebral cortex when rats were acutely exposed to malathion and zinc, demonstrating that the research on gender-related differences in health effects caused by xenobiotic and ⁄ or essential elements requires further attention.Gender-based differences in the metabolism constitute a major topic in biology, and sex-dependent toxicity permeates the literature for a series of factors. Some examples of research areas where gender differences are important determinants of toxicity are: metal toxicity [1], pharmacokinetics [2], hormone metabolism [3], xenobiotics metabolism [4] and traumatic injury vulnerability [5]. The relevance of studying gender-dependent toxicity has been stressed before: 'Gender may be the most important factor in mammalian development and response to exogenous agents' [6].Incidental or intentional organophosphate intoxication is a relevant health problem in developing countries [7]. Despite the limitation of population analysis, neurobehavioural impairment might be the consequence of an acute poisoning, and possibly the consequence of relatively high and prolonged exposure [8]. Organophosphate has been considered as an important risk factor for depression and correlated to suicide attempts [9] and has been used as a model of depressive-like behaviour in animals [10]. Malathion, a pesticide widely used to fight fleas, lice, mosquitoes and flies, is thought to be one of the main agents leading to human organop...

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“…Moreover, many authors postulate that these compounds, both in acute and chronic intoxication, change the activities of antioxidative enzymes and cause enhancement of lipid peroxidation in the kidney, liver and brain [6][7][8][9][10][11][12]. However, changes in lipid peroxidation index in different organs are due to for example, exposure duration.…”

Section: Introductionmentioning

confidence: 99%

Changes in antioxidative parameters in the kidney of rats subchronically intoxicated with chlorfenvinphos — an organophosphate insecticide

Lukaszewicz-Hussain

2009

Open Medicine

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AbstractChlorfenvinphos is an organophosphate insecticide, posing a risk to those who are professionally involved in its production and use in agriculture, as well as to the general population. Organophosphates (OPs) are the class of insecticides, whose primary target is acetylcholinesterase (AChE) that hydrolyzes acetylcholine, a major neurotransmitter at the central and peripheral neuronal synapses. Moreover, many authors postulate that these compounds, both in acute and chronic intoxication, change the activities of antioxidative enzymes, thus leading to the enhancement of lipid peroxidation in many tissues. In the current study, animals received once a day, intragastrically with a stomach tube, 0.1ml/100g of olive oil (control groups) and oil solution of chlorfenvinphos at a dose of 0.02LD50 (0.3 mg/kg b. w.) — the experimental groups. The animals were sacrificed on day 14 or on day 28 of exposure. In the kidneys of rats, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) as well as reduced glutathione level (GSH) were determined. Chlorfenvinphos administration resulted in increased activities of antioxidative enzymes in the kidney of rats. Renal activities of SOD, GPx and GR were more pronounced on day 28 of chlorfenvinphos exposure than on day 14. The kidney reduced glutathione level (GSH) did not change in comparison to the control level. The current experimental findings indicate that subchronic administration of chlorfenvinphos leads to an adaptive response in the kidney of rats and this response is mostly due to reduced glutathione level and glutathione metabolism.

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Lipid peroxidative damage on malathion exposure in rats

Cited by 58 publications

References 35 publications

Protective Effects of Manassantin A against Ethanol-Induced Gastric Injury in Rats

Protective Effects of Manassantin A against Ethanol-Induced Gastric Injury in Rats

Gender Effects of Acute Malathion or Zinc Exposure on the Antioxidant Response of Rat Hippocampus and Cerebral Cortex

Changes in antioxidative parameters in the kidney of rats subchronically intoxicated with chlorfenvinphos — an organophosphate insecticide

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