Deltamethrin induces mitochondrial membrane permeability and altered expression of cytochrome C in rat brain

Abstract

Deltamethrin is a type II synthetic pyrethroid insecticide and is used extensively. Numerous studies have demonstrated that deltamethrin can cause severe central nervous system symptoms. The mechanism of neuro-toxicity caused by deltamethrin is still poorly understood. This study investigated the effect of deltamethrin on the mitochondria-mediated apoptosis pathway in rat brain. The cortex and hippocampus mitochondrial membrane potential, permeability transition, expression of cytochrome c and activity of cytochrome c oxidase was assayed at 5, 24, 48 and 72 h following deltamethrin treatment. The study observed that the membrane potential, change of absorbance at 540 nm (A(540)), intensities of cytochrome c in mitochondria and activity of cytochrome c oxidase in the cortex and hippocampus of treated groups were significantly lower than those of the control group. The results of the study demonstrated that deltamethrin induced a decreased mitochondrial membrane potential and increased permeability, and reduced the expression of cytochrome c, thus depressing the activity of cytochrome c oxidase significantly. It indicates that deltamethrin may have an effect on mitochondria-mediated apoptosis of nerve cells in the rat brain.

Maternal inheritance of deltamethrin resistance in the salmon louse Lepeophtheirus salmonis (Krøyer) is associated with unique mtDNA haplotypes

“…In rodent models, deltamethrin further affected mitochondrial functions other than respiration. In particular, deltamethrin activated mitochondrial apoptotic pathways in rat brain cells [48] and disrupted steroid biosynthesis in mouse Leydig cells by causing mitochondrial membrane damage [49]. …”

The Effects of Taurine on Permethrininduced Cytogenetic and Oxidative Damage in Cultured Human Lymphocytes

“…Pyrethroid pesticides have recently been reported to cause apoptosis (47), disrupt the endocrine system (48), change nitrogen metabolism (49), increase mitochondrial membrane permeability (50), and alter constitutive nitric oxide release (51). Higher SCE and MN frequencies and higher TOS plasma levels in our study confi rm the genotoxic and oxidative action of PM in human lymphocytes.…”

Tryptophan fluorescence quenching as a binding assay to monitor protein conformation changes in the membrane of intact mitochondria

“…Earlier studies have shown that organophosphates (Kashyap et al 2010), carbamates (Li et al 2015) and organochlorine (Kitazawa et al 2003) insecticides induce apoptosis through mitochondrial-dependent pathway, and similar indications were obtained in the present study. In vivo exposure of a synthetic pyrethroid -deltamethrin, have been shown to reduce mitochondrial cytochrome c levels (Chen et al 2007), and induce apoptosis through mitochondrial-independent pathway. Deltamethrin-induced apoptosis is initiated through a mitochondrial-independent pathway due to its interaction with Na + channels, leading to calcium overload and activation of the endoplasmic reticulum (ER) stress pathway (Hossain and Richardson 2011).…”