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

Abstract

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.

Immunological and genotoxic effects of occupational exposure to α-cypermethrin pesticide

“…The finding that the highly exposed group of workers had lower CD4/CD8 as compared to the unexposed group was in agreement with a cross-sectional study of CYP occupational exposures, which found that exposed workers had lower level of CD4% and CD4/CD8% as compared to other less or not exposed groups [21]. Although the reference range for normal value was not exceeded in both studies but the possibility of immune system imbalance diseases as Parkinsonism as a result of oxidative stress caused by CYP exposure [27]. The current study investigated the effect of socio-demographic and occupational factors on oxidative stress, genotoxicity and immunological disturbances among exposed workers.…”

Effects of exposure to pyrethroid cyfluthrin on serotonin and dopamine levels in brain regions of male rats

“…Oxidative stress has been a matter of concern in the pathogenesis of neurodegenerative diseases (Patel et al, 2006;Gupta et al, 2010). Recently, Tripathi et al (2014) showed that the pyrethroid cypermethrin decreased the striatal dopamine content by altering the status of oxidative stress indicators and antioxidant defense system; this mechanism of oxidative stress might be of value for predicting the nigrostriatal dopaminergic neurodegeneration and the nigrostriatal toxicity related to neurological disorders (Fig. 3).…”

Pyrethroid exposure and neurotoxicity: a mechanistic approach

“…Singh et al (19) identified higher nitrite (an indicator of nitrosamine stress) and lipid peroxide (LPO, an indicator of oxidative stress) levels in the nigrostriatum. Nitrite and LPO were also significantly increased in the peripheral blood of rats exposed to cypermethrin dose that induces nigrostriatal dopaminergic neurodegeneration (26).…”