Early life permethrin insecticide treatment leads to heart damage in adult rats

Vadhana, M.S. Dhivya; Carloni, Manuel; Nasuti, Cinzia; Fedeli, Donatella; Gabbianelli, Rosita

doi:10.1016/j.exger.2011.05.005

Cited by 53 publications

(21 citation statements)

References 46 publications

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“…; Vadhana et al . ). The reactive oxygen species (ROS) generation and malondialdehyde (MDA) production were increased by PM treatment, while the activity of antioxidant enzymes such as catalase and superoxide dismutase and glutathione content had declined in the rats (Hu et al .…”

Section: Discussionmentioning

confidence: 97%

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Efficacy of naringenin against permethrin‐induced testicular toxicity in rats

Mostafa

El-Baset

Kattaia

et al. 2016

Int J Experimental Path

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SUMMARYPermethrin (PM), a synthetic pyrethroid insecticide, has broad toxicity spectra. We aimed to investigate the effects of PM on the testes of adult albino rats, examine the recovery response and evaluate the efficacy of naringenin (NG) supplementation. Adult male albino rats were randomly assigned to five groups of six each: control, NG (50 mg/kg), PM (70 mg/kg), recovery (after subsequent withdrawal of PM) and NG-PM group. All treatments were given by oral gavage for 6 weeks and another 3 weeks for the recovery group. At the time of sacrifice, each testis was weighed. Biochemical analysis of epididymal sperm count and serum testosterone level was performed. Testes were processed for histological, ultrastructural and c-Kit immunohistochemical study. PM toxicity was evidenced by a highly significant decrease in testicular weight, epididymal sperm count and serum testosterone level compared to control. Furthermore, testicular structure abnormalities and reduced c-Kit immunoreactions were observed. Stoppage of PM in the recovery group partially reversed PMinduced changes. There was a mild decrease in testicular weight and biochemical parameters compared to control. The structure of seminiferous tubules was partially retained. The NG-PM group showed an overall improvement in testicular weight and biochemical alterations which were confirmed by light and electron microscopic examination. In conclusion, PM induced testicular toxicity, which was ameliorated by NG co-administration. However, stoppage of PM exposure was associated with partial recovery.

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Section: Discussionmentioning

confidence: 97%

“…), heart damage (Vadhana et al . ), neurological disorders and behavioural changes (Wolansky & Harrill ; Carloni et al . ).…”

mentioning

confidence: 99%

Efficacy of naringenin against permethrin‐induced testicular toxicity in rats

Mostafa

El-Baset

Kattaia

et al. 2016

Int J Experimental Path

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“…These studies generally used high toxic doses [32]. The documented toxicity of permethrin and DEET includes testicular histopathological damage [33], uterine enlargement, atrophy of male secondary sex organs [6], testicular cancer [7], liver damage [34], heart damage [35], neurological disorders and behavioral changes [8–10], oxidative stress in brain [11], DNA damage [12] and immunotoxicity [13]. The current study was designed to examine the actions of pharmacological doses of the pesticide mixture compounds on epigenetic transgenerational inheritance of adult-onset disease.…”

Section: Discussionmentioning

confidence: 99%

Pesticide and insect repellent mixture (permethrin and DEET) induces epigenetic transgenerational inheritance of disease and sperm epimutations

Manikkam¹,

Tracey²,

Guerrero-Bosagna³

et al. 2012

Reproductive Toxicology

188

150

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Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a “pesticide mixture” (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures.

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“…Preparation of heart cells The hearts were collected, rinsed with ice‐cold PBS, and the ventricles were dissected into small fragments using a surgical blade (Vadhana et al 2010, 2011 a , b ). The samples were then homogenized in a glass tube with a pestle and extensively washed again in cold PBS until blood cells were not observed and then minced using 0.9% NaCl.…”

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confidence: 99%

Exercise‐induced heart mitochondrial cholesterol depletion influences the inhibition of mitochondrial swelling

Ziółkowski

Vadhana²,

Kaczor

et al. 2013

Experimental Physiology

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New findings r What is the central question of this study?The central question was to establish whether decreased cholesterol content in heart mitochondria caused by prolonged swimming may provoke changes in their bioenergetics and affect resistance to CaCl 2 -induced mitochondrial swelling. r What is the main finding and its importance?The main finding is the indication that changes in the cholesterol pool in heart mitochondria induced by swimming exercise are related to an increase in resistance to CaCl 2 -induced swelling, probably by remodelling of lipid microdomains, and are not deleterious for mitochondrial bioenergetics. These findings may contribute to a more complete understanding of the defense system that may prevent mitochondrial degradation during exercise and the protective system of cardiac cell defense in stress conditions. The significance of the reduction of the cholesterol pool in heart mitochondria after exercise is still unknown. Recently, published data have suggested that cholesterol may influence the components of mitochondrial contact site and affect mitochondrial swelling. Therefore, the aim of this study was to determine whether the decreased cholesterol content in heart mitochondria caused by prolonged swimming may provoke changes in their bioenergetics and result in an increased resistance to calcium chloride-induced mitochondrial swelling. Male Wistar rats were divided into a sedentary control group and an exercise group. The rats exercised for 3 h, burdened with an additional 3% of their body weight. Their hearts were removed immediately after completing the exercise. The left ventricle was divided and used for experiments. Mitochondrial cholesterol content, membrane fluidity and mitochondrial bioenergetics were measured in the control and exercised rat heart mitochondria. To assess whether mitochondrial modifications are linked to disruption of lipid microdomains, methyl-β-cyclodextrin, a well-known lipid microdomain-disrupting agent and cholesterol chelator, was applied to the mitochondria of the control group. Cholesterol depletion, increased membrane fluidity and increased resistance to calcium chloride-induced swelling were observed in postexercise heart crude mitochondrial fraction. Similar results were achieved in control mitochondria treated with 2% methyl-β-cyclodextrin. All of the mitochondrial bioenergetics parameters were similar between the groups.

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Early life permethrin insecticide treatment leads to heart damage in adult rats

Cited by 53 publications

References 46 publications

Efficacy of naringenin against permethrin‐induced testicular toxicity in rats

Efficacy of naringenin against permethrin‐induced testicular toxicity in rats

Pesticide and insect repellent mixture (permethrin and DEET) induces epigenetic transgenerational inheritance of disease and sperm epimutations

Exercise‐induced heart mitochondrial cholesterol depletion influences the inhibition of mitochondrial swelling

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