Effects of cypermethrin on monoamine transporters, xenobiotic metabolizing enzymes and lipid peroxidation in the rat nigrostriatal system

Tiwari, Manindra Nath; Singh, Anand Kumar; Ahmad, Israr; Upadhyay, Ghanshyam; Singh, Dhirendra Kumar; Patel, Devendra Kumar; Singh, Chetna; Prakash, Om; Singh, Mahendra Pratap

doi:10.3109/10715762.2010.512041

Cited by 45 publications

(27 citation statements)

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“…Cypermethrin increased nitrite content and LPO in the plasma, platelets and PMNs, which suggest that it induces toxicity in the peripheral system that could possibly be correlated with oxidative stress indicators in the nigrostriatal tissues of toxin-induced PD [5,13,25,32]. Free radicals generated owing to cypermethrinmediated intoxication attack the biological membrane leading to lipid peroxidation [32].…”

Section: Discussionmentioning

confidence: 99%

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Cypermethrin alters the status of oxidative stress in the peripheral blood: relevance to Parkinsonism

et al. 2014

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Parkinson's disease (PD) is a motor scarcity disorder characterized by the striatal dopamine deficiency owing to the selective degeneration of the nigrostriatal dopaminergic neurons. While oxidative stress is implicated in PD, prolonged exposure to moderate dose of cypermethrin induces Parkinsonism. The study aimed to investigate the status of oxidative stress indicators and antioxidant defence system of the polymorphonuclear leukocytes (PMNs), platelets and plasma to delineate the effect of Parkinsonian dose of cypermethrin in the peripheral blood of rats and its subsequent relevance to Parkinsonism. Nitrite content, lipid peroxidation (LPO) and activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR) and glutathione-S-transferase (GST) were measured in the PMNs, platelets and plasma of control and cypermethrin-treated rats in the presence or absence of a microglial activation inhibitor, minocycline or a dopamine precursor containing the peripheral 3,4-dihydroxyphenylalanine decarboxylase inhibitor, named syndopa, employing the standard procedures. The striatal dopamine was measured to assess the degree of neurodegeneration/neuroprotection. Cypermethrin increased nitrite and LPO in the plasma, platelets and PMNs while it reduced the striatal dopamine content. Catalase and GST activity were increased in the PMNs and platelets; however, it was reduced in the plasma. Conversely, SOD and GR activities were reduced in the PMNs and platelets but increased in the plasma. Minocycline or syndopa reduced the cypermethrin-mediated changes towards normalcy. The results demonstrate that cypermethrin alters the status of oxidative stress indicators and impairs antioxidant defence system of the peripheral blood, which could be effectively salvaged by minocycline or syndopa. The results could be of value for predicting the nigrostriatal toxicity relevant to Parkinsonism.

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Section: Discussionmentioning

confidence: 99%

“…LPO Cells/plasma was mixed with SDS (10 % w/v) and acetic acid (20 % v/v). The reaction mixture was incubated, and TBA (0.8 % w/v) was added and boiled for 1 h [32] and then centrifuged at 4°C. The absorbance of the supernatant was recorded at 532 nm against blank.…”

Section: Nitrite Estimationmentioning

confidence: 99%

Cypermethrin alters the status of oxidative stress in the peripheral blood: relevance to Parkinsonism

et al. 2014

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“…We are exposed to many chemicals, such as heavy metals and pyrethroid pesticides in our daily life; therefore, these chemicals are being employed to develop the animal models. Melatonin is not yet checked against metals and cypermethrin-induced nigrostriatal dopaminergic neurodegeneration, as these are relatively newer animal models [94][95][96][97].…”

Section: Other Rodent Models and Melatoninmentioning

confidence: 98%

Melatonin as a Neuroprotective Agent in the Rodent Models of Parkinson’s Disease: Is it All Set to Irrefutable Clinical Translation?

et al. 2011

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Parkinson's disease (PD), a neurodegenerative disorder, is characterized by the selective degeneration of the nigrostriatal dopaminergic neurons, continuing or permanent deficiency of dopamine, accretion of an abnormal form of alpha synuclein in the adjacent neurons, and dysregulation of ubiquitin proteasomal system, mitochondrial metabolism, permeability and integrity, and cellular apoptosis resulting in rigidity, bradykinesia, resting tremor, and postural instability. Melatonin, an indoleamine produced almost in all the organisms, has anti-inflammatory, anti-apoptotic, and anti-oxidant nature. Experimental studies employing 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), methamphetamine, rotenone, and maneb and paraquat models have shown an enormous potential of melatonin in amelioration of the symptomatic features of PD. Although a few reviews published previously have described the multifaceted efficacy of melatonin against MPTP and 6-OHDA rodent models, due to development and validation of the newer models as well as the extensive studies on the usage of melatonin in entrenched PD models, it is worthwhile to bring up to date note on the usage of melatonin as a neuroprotective agent in PD. This article presents an update on the usage and applications of melatonin in PD models along with incongruous observations. The impending implications in the clinics, success, limitations, and future prospective have also been discussed in this article.

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“…Firstly, in some of the occupational and laboratory studies using PQ to induce PS, the pathophysiology of this disease have been unraveled [4] . For example, rotenone and PQ are in the same group of herbicide that causes mitochondrial dysfunction and massive oxidative stress [5][6][7][8] , which for some reasons, PQ or rotenone has been considered to be greatly advantageous in animal models of PS, giving a likelihood of gradual loss of neurons that depict the disease. However, 6-OHDA and MPTP models are seemed to be very useful for targeting and for destroying the DA neurons rapidly, notwithstanding, this does not demonstrate how it usually take a long duration before developing PS in human [2,9].…”

Section: Discussionmentioning

confidence: 99%

“…Fig 8 shows the number of mice that survival PQ challenged after the behavioral tests, the values represent the numbers of mice that were counted and expressed in percentage.…”

Section: Asa and Pred Increased Survival In Treatment Groupsmentioning

confidence: 99%

In Invivo model of Parkinson’s syndrome, concurrent administrations of anti-inflammatory drugs changed behavioral deficits

Oluwole

Olajire²

2015

Inflamm Cell Signal

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In most of the laboratory and occupational studies, Parkinson's syndrome (PS) is the major outcome of paraquat (PQ) toxicities. Nevertheless, the search for novel therapy against PS is still enormous. We therefore examined the effects of anti-inflammatory drugs against PS. Swiss mice (30-35g) were pretreated orally with saline, distilled water, acetylsalicylate acid (10mg/kg) or prednisolone (5mg/kg) for 7days. They were concurrently treated for another 5 weeks against intraperitoneal injection of 0.01ml and 0.02ml of (10mg/kg) PQ which were given twice a week to induced PS. Subsequently, movement deficits in mice were closely examined by using the spontaneous motor activity test, the catalepsy, and hanging tests. Thereafter, the mice brains were dissected for the biochemical tests. The data were analyzed using ANOVA, and the values were statistically significant at (p<0.0001, p<0.05). In conclusion, aspirin and prednisolone produced strong antioxidant effects that may be associated with change in the behavioral deficits.

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Effects of cypermethrin on monoamine transporters, xenobiotic metabolizing enzymes and lipid peroxidation in the rat nigrostriatal system

Cited by 45 publications

References 53 publications

Cypermethrin alters the status of oxidative stress in the peripheral blood: relevance to Parkinsonism

Cypermethrin alters the status of oxidative stress in the peripheral blood: relevance to Parkinsonism

Melatonin as a Neuroprotective Agent in the Rodent Models of Parkinson’s Disease: Is it All Set to Irrefutable Clinical Translation?

In Invivo model of Parkinson’s syndrome, concurrent administrations of anti-inflammatory drugs changed behavioral deficits

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