Lufenuron induces reproductive toxicity and genotoxic effects in pregnant albino rats and their fetuses

Abstract

Insecticides and other agrochemicals have become indispensable components of the agricultural system to ensure a notable increase in crop yield and food production. As a natural consequence, chemical residues result in significantly increased contamination of both terrestrial and aquatic ecosystems. The present study evaluated the teratogenic, genotoxic, and oxidative stress effects of residual-level lufenuron exposure on pregnant rats during the organogenesis gestational period of both mother and fetus. The tested dams were divided into three groups; control (untreated), low-dose group (orally administered with 0.4 mg/kg lufenuron) and high-dose group (orally administered with 0.8 mg/kg lufenuron). The dams of the two treatment groups showed teratogenic abnormalities represented by the asymmetrical distribution of fetuses in both uterine horns, accompanied by observed resorption sites and intensive bleeding in the uterine horns, whereas their fetuses suffered from growth retardation, morphologic malformations, and skeletal deformations. Histologic examination of the liver and kidney tissues obtained from mothers and fetuses after lufenuron exposure revealed multiple histopathologic changes. DNA fragmentation and cell cycle perturbation were also detected in the liver cells of lufenuron-treated pregnant dams and their fetuses through comet assay and flow cytometry, respectively. Moreover, lufenuron-induced oxidative stress in the liver of mothers and fetuses was confirmed by the increased malondialdehyde levels and decreased levels of enzymatic antioxidants (glutathione peroxidase and superoxide dismutase). Taken together, it can be concluded that lufenuron has a great potential in exerting teratogenic, genotoxic, and oxidative stresses on pregnant rats and their fetuses upon chronic exposure to residual levels during the organogenesis gestational period. The obtained results in the present study imply that women and their fetuses may have the same risk.

Toxicopathological and Molecular Studies on Imidacloprid and Hexaflumuron-induced Hepatorenal Toxicity in Rats.

“…In addition, severe hepatotoxicity has been reported to induce hepatoencephalopathic neurobehavioral alterations (Hayase et al 2000) The results of the present study revealed that IC and HFM induced hepatorenal oxidative stress damage manifested by increased MDA levels and decreased TAC levels associated with the upregulation of HO-1 gene and down-regulation of Keap1 gene levels. These ndings agreed with other report showed that lufenuron, belonging to the same hexa umuron-family, was able to induce oxidative stress damage in the liver of rats (Basal et al 2020). Also, chronic exposure to IC alters in ammation and oxidative stress markers…”

Paternal Fenitrothion Exposures in Rats Causes Sperm DNA Fragmentation in F0 and Histomorphometric Changes in Selected Organs of F1 Generation

“…Epigenetic changes are necessary to direct normal cellular development and differentiation in developing organisms, however, developmental abnormalities may occur in response to inappropriate epigenetic signaling [ 76 ]. Besides, maternal exposure to lufenuron, an insecticide, during organogenesis had caused glomerular shrinkage in the progenies, which might be due to the genotoxic stress and cell cycle arrest of this insecticide [ 77 ]. This might explain the possible mechanism involved in the paternal exposure of FNT, which caused glomerulus shrinkage in the male F1 progeny rats.…”

Exposure to Lufenuron During the Third Gestational Period Induces Genotoxicity and Oxidative Stress Effects in Pregnant Albino Rats and Their Fetuses

“…Thiacloprid-based insecticide treatment resulted in p53-mediated cell cycle arrest at the G0/G1 phase, and apoptosis induction in bovine lymphocytes (Schwarzbacherová et al, 2019). In a more recent study carried out in our labs, exposure of pregnant albino rats to lufenuron during the organogenesis period led to cell cycle arrest in liver cells of both mothers and fetuses at the G0/G1 phase (Basal et al, 2020).…”

“…It also interfered with the formation of spindle fibers in spermatid cells of mice (Deivanayagam et al, 2013) along with the induction of molecular lesions in the mice genome (Abou Gabal, 2006). At the DNA level, comet assay revealed significant damage in hepatocytes of female rats and their fetuses (Basal et al, 2020), fruit fly (Eid et al, 2017) and freshwater snails (Ibrahim et al, 2018) after treatment with lufenuron. The same results were obtained in vivo after treatment of mice peripheral blood lymphocytes to carbofuran (Pei et al, 2005).…”