Abstract
The pyrethroid toxicants, fatal at high doses, are found as remnants of crop pesticides and ingredients of commercially available insecticides. The toxic effects of high-content insecticidal pyrethroid formulations are available in 0.05 g, 1.17 g, and 0.04 g pyrethroid-instilled products, namely burning coils, pyrethroid-soaked mats, and liquid formulations of pyrethroids that release pyrethroid vapor/smoke upon heating. They provided 5.46 g/kg, 21.15 g/kg, and 4.24 g/kg of toxicants to the experimental animals over a total of 3 weeks/5 h per os (p.o.) administration, producing necrosis, hyperemia, and fatty changes in the liver; fiber separation in cardiac muscles; atrophy, lymphatic infiltration, blood vessel congestion, and hyperemia in the heart tissues of the experimental animals. The glomerular tuft necrosis, cytoplasmic degeneration of renal tubular cells, necrotic tubules, congestion, and dilatation of blood vessels were observed in the kidney tissue of intoxicated animals. Air-space enlargement, interstitial inflammation, lymphocyte infiltration aggregates, connective tissue infiltration by inflammatory cells, and hyperemia were found in the lung tissues. The pyrethroid toxicants also produced nervous tissue degeneration and decreased neurons in the brain, which were observed through histopathological examinations of the brain, lungs, heart, kidneys, and liver. The protective effects of ascorbic acid (AA/vitamin C) and α-tocopherol (E307/vitamin E) at 100 mg/kg oral doses administered daily for the entire period of the toxicant exposure of three weeks to the experimental mice, aged between 3–4 months and weighing ≈30 g, ameliorated the tissue damage, as observed through the histopathological examinations. The ascorbic acid caused recovery of the liver, kidney, brain, and heart tissue damage, while α-tocopherol was effective at ameliorating the damage in the kidneys and lung tissue compared with the control groups. The high levels of tissue damage recovery suggested a prophylactic effect of the concurrent use of ascorbic acid and α-tocopherol for the subjects under the exposure of pyrethroids.
Highlights
Pyrethroid toxicants are found in contaminated fruits, vegetables, and other foodstuffs, including grains as remnants of crops, produce after pyrethroid pesticide use [1], and as ingredients of various commercially available insecticidal products [2]
The pyrethroid-exposed and treated groups’ analysis showed the significant role of anti-oxidants, namely ascorbic acid (AA) and α-tocopherol (EA307), via their ability to ameliorate the toxic effects in the studied groups of experimental animals
The results were comprehensively analyzed using statistical methods, and the values presented in the analysis are expressed as mean ± standard error (SE) followed by p-values obtained from Dunnett’s corrections, as well as 95% confidence intervals
Summary
Pyrethroid toxicants are found in contaminated fruits, vegetables, and other foodstuffs, including grains as remnants of crops, produce after pyrethroid pesticide use [1], and as ingredients of various commercially available insecticidal products [2]. High and alarming levels of pyrethroid residues have recently been detected in the environment, including in sediment samples and agricultural land areas from developed countries [4] In this context, the presence of pesticidal residues in the environment, especially regarding exposures in the residential and other habitable localities, produce infiltration-induced side effects in humans, exposed children, pregnant women, and farm and garden/orchard workers need more attention [5]. The presence of pesticidal residues in the environment, especially regarding exposures in the residential and other habitable localities, produce infiltration-induced side effects in humans, exposed children, pregnant women, and farm and garden/orchard workers need more attention [5] Another source of contamination of pyrethroids on a large scale is humans’ use of pesticidal ingredients, such as mosquito repellants in underdeveloped and developing countries [6]. The continued exposure may affect vital organs, leading to organ malfunction and cause high toxicity in the affected subjects at temporary and permanent timescales depending upon the duration and dose of the toxicants [7]
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