Mitochondrial ATP synthase inhibition and nitric oxide are involved in muscle weakness that occurs in acute exposure of rats to monocrotophos

Venkatesh, Sriram; Ramachandran, Anup; Zachariah, Anand; Oommen, Anna

doi:10.1080/15376510802455354

Cited by 22 publications

(19 citation statements)

References 32 publications

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“…[140][141][142] Depression of NADH cytochrome c reductase, succinate cytochrome c reductase, and CcOX activity in the mitochondrial respiratory chain, reduction of mitochondrial transmembrane potential and ATP concentration, elevation of ADP/ATP ratio, induction of LDH release, and necrotic cell death occurred following OP poisoning. [143][144][145][146] Moreover, this pesticide induced cholinergic receptor-independent necrotic cell death. Reduction of SDH and elevation of LDH suggest that anaerobic metabolism was favored while aerobic oxidation of pyruvate was impaired after OP exposure.…”

Section: Musclementioning

confidence: 99%

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

2010

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Pesticides, including organophosphate (OP), organochlorine (OC), and carbamate (CB) compounds, are widely used in agricultural and indoor purposes. OP and CB act as acetyl cholinesterase (AChE) inhibitors that affect lots of organs such as peripheral and central nervous systems, muscles, liver, pancreas, and brain, whereas OC are neurotoxic involved in alteration of ion channels. There are several reports about metabolic disorders, hyperglycemia, and also oxidative stress in acute and chronic exposures to pesticides that are linked with diabetes and other metabolic disorders. In this respect, there are several in vitro and in vivo but few clinical studies about mechanism underlying these effects. Bibliographic databases were searched for the years 1963–2010 and resulted in 1652 articles. After elimination of duplicates or irrelevant papers, 204 papers were included and reviewed. Results indicated that OP and CB impair the enzymatic pathways involved in metabolism of carbohydrates, fats and protein within cytoplasm, mitochondria, and proxisomes. It is believed that OP and CB show this effect through inhibition of AChE or affecting target organs directly. OC mostly affect lipid metabolism in the adipose tissues and change glucose pathway in other cells. As a shared mechanism, all OP, CB and OC induce cellular oxidative stress via affecting mitochondrial function and therefore disrupt neuronal and hormonal status of the body. Establishing proper epidemiological studies to explore exact relationships between exposure levels to these pesticides and rate of resulted metabolic disorders in human will be helpful.

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Section: Musclementioning

confidence: 99%

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

2010

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“…Since, there are limited data about the hepatotoxicity of OPs in humans, it is not certain whether changes in biochemical parameters indicate actual liver damage. (90)(91)(92)(93)(94), energy production (93,(95)(96)(97), and cell death (98)(99)(100). Several studies have found an association between mitochondrial dynamics and malathion-induced drop in mitochondrial ATP synthesis in rat liver (9) or quinalphos and acephate effects on liver succinic dehydrogenase (84,85,101) and ATPase activities (87) -all of them the key enzymes for oxidative phosphorylation.…”

Section: Biochemical Evidence Of Op Hepatotoxicitymentioning

confidence: 99%

Adverse effects of organophosphorus pesticides on the liver: a brief summary of four decades of research

Karami‐Mohajeri

Ahmadipour

Rahimi

et al. 2017

Archives of Industrial Hygiene and Toxicology

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Organophosphorus pesticides (OPs) are widely used volatile pesticides that have harmful effects on the liver in acute and chronic exposures. This review article summarises and discusses a wide collection of studies published over the last 40 years reporting on the effects of OPs on the liver, in an attempt to propose general mechanisms of OP hepatotoxicity and possible treatment. Several key biological processes have been reported as involved in OP-induced hepatotoxicity such as disturbances in the antioxidant defence system, oxidative stress, apoptosis, and mitochondrial and microsomal metabolism. Most studies show that antioxidants can attenuate oxidative stress and the consequent changes in liver function. However, few studies have examined the relationship between OP structures and the severity and mechanism of their action. We hope that future in vitro, in vivo, and clinical trials will answer the remaining questions about the mechanisms of OP hepatotoxicity and its management.

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“…32 Increased level of NO is a natural sequence to the inhibition of AChE by OPs. 9 The results showed that there is a significant increase in nitrate (measured as nitrite) in plasma and lung in MP-treated group. Therefore, we make a conclusion that the change of NO level is harmful to lung tissue.…”

Section: Discussionmentioning

confidence: 94%

Protective effect of sodium aescinate on lung injury induced by methyl parathion

Wang

Jiang

et al. 2010

Hum Exp Toxicol

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Methyl parathion (MP) is a high venenosus insecticide. It has been used in pest control of agriculture for several years. The present study is performed to investigate the protective effect of sodium aescinate (SA) on lung injury induced by MP. Forty male Sprague-Dawley rats are randomly divided into five groups, with 8 animals in each group: control group, MP administration group, MP plus SA at doses of 0.45 mg/kg, 0.9 mg/kg and 1.8 mg/kg groups. Acetylcholinesterase (AChE) activity and nitric oxide (NO) level in plasma, myeloperoxidase (MPO) activity, NO level, and antioxidative parameters in lung tissue are assayed. Histopathological examination of lung is also performed. The results show that SA has no effect on AChE. Treatment with SA decreases the activity of MPO in lung and the level of NO in plasma and lung. The level of malondialdehyde in lung is decreased after SA treatments. SA increases the activities of superoxide dismutase, glutathione peroxidase and the content of glutathione in lung. SA administration also ameliorates lung injury induced by MP. The findings indicate that SA could protect lung injury induced by MP and the mechanism of action is related to the anti-inflammatory and anti-oxidative effect of SA.

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Mitochondrial ATP synthase inhibition and nitric oxide are involved in muscle weakness that occurs in acute exposure of rats to monocrotophos

Cited by 22 publications

References 32 publications

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

Toxic influence of organophosphate, carbamate, and organochlorine pesticides on cellular metabolism of lipids, proteins, and carbohydrates

Adverse effects of organophosphorus pesticides on the liver: a brief summary of four decades of research

Protective effect of sodium aescinate on lung injury induced by methyl parathion

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