El Gazzar Walaa Bayoumie, Bayoumi Heba, Youssef Heba S, Ibrahim Tayseer A, Abdelfatah Reham M, Gamil Noha M, Iskandar Mervat K, Abdel-Kareim Amal M, Abdelrahman Shaymaa M, Gebba Mohammed A, Mohamed Mona Atya, Mokhtar Maha M, Kharboush Tayseir G, Bayoumy Nervana M, Alomar Hatun A, Farag Amina A
Department of Anatomy, Physiology and Biochemistry, Faculty of Medicine, The Hashemite University, P.O. Box 330127, Zarqa 13133, Jordan.
Department of Medical Biochemistry & Molecular Biology, Faculty of Medicine, Benha University, Benha 13518, Egypt.
Toxics. 2024 Jun 21;12(7):445. doi: 10.3390/toxics12070445.
Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following oral consumption of imidacloprid neonicotinoids (45 mg/kg daily for 30 days) and the potential protective effects of lycopene (LYC) administration (10 mg/kg/day for 30 days) with IMI exposure in male Sprague-Dawley rats. The apoptotic, pyroptotic, inflammatory, oxidative stress, and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, inflammatory, pyroptotic, and apoptotic biomarkers were also observed following IMI administration. LYC effectively reversed these alterations by reducing oxidative stress markers (e.g., MDA) and enhancing antioxidant enzymes (SOD, CAT). It downregulated ER stress markers (IRE1α, XBP1, CHOP), decreased pro-inflammatory cytokines (TNF-α, IL-1β), and suppressed pyroptotic (NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the histopathological and ultrastructure alterations brought on by IMI toxicity.
吡虫啉（IMI）是一种常用的新一代农药，对包括动物在内的非靶标生物有诸多有害影响。本研究分析了雄性Sprague-Dawley大鼠口服吡虫啉类新烟碱（每天45毫克/千克，持续30天）后对胰腺的不良影响，以及番茄红素（LYC）给药（每天10毫克/千克，持续30天）在IMI暴露情况下的潜在保护作用。评估了凋亡、焦亡、炎症、氧化应激和内质网应激生物标志物，以及组织病理学改变。给予IMI后，胰腺组织病理学出现明显变化。此外，给予IMI后还观察到氧化/内质网相关应激生物标志物、炎症、焦亡和凋亡生物标志物升高。LYC通过降低氧化应激标志物（如丙二醛）和增强抗氧化酶（超氧化物歧化酶、过氧化氢酶）有效逆转了这些改变。它下调了内质网应激标志物（肌醇需求酶1α、X盒结合蛋白1、C/EBP同源蛋白），降低了促炎细胞因子（肿瘤坏死因子-α、白细胞介素-1β），并抑制了焦亡（NOD样受体蛋白3、半胱天冬酶-1）以及凋亡标志物（Bax、裂解的半胱天冬酶-3）。它还改善了IMI毒性引起的组织病理学和超微结构改变。
