The present study investigated the alleviating role of camel milk (CM) in the mitigation of fenpropathrin (FNP) type II pyrethroid induced oxidative stress, alterations of hepatic (CYP1A1) mRNA expression pattern, and DNA damage using the alkaline comet assay (SCGE) in male rats. Sixty male Sprague-Dawley rats were separated into six groups (n = 10): 1st control (C), 2nd corn oil (CO), 3rd (CM): gavaged CM 2ml/rat, 4th (FNP): gavaged FNP 7.09 mg/kg body weight (BW), 5th (FNP pro/co-treated): gavaged CM firstly for 15 days, then CM + FNP by the same mentioned doses and route, 6th (FNP + CM co-treated): gavaged FNP firstly followed by CM by the same mentioned doses and route. Rats were orally gavaged three times per week, day after day for 60 days. FNP exposure significantly reduced serum glutathione (GSH) levels, but significantly increased serum levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), protein carbonyl (PCO), and 8hydroxy2deoxyguanosine (8OH2dG). Additionally, FNP exposure significantly up-regulated the mRNA expression levels of hepatic CYP1A1 and increased the SCGE indices in whole blood, liver, and spleen tissues of exposed male rats. Administration of CM significantly regulated the FNP induced oxidative stress, reduced hepatic CYP1A1 mRNA expression levels and values of comet assay indices particularly in the (CM + FNP pro/co-treated) group compared to the (FNP + CM co-treated) group. In conclusion, our results indicate, for the first time, that FNP retains an in vivo genotoxic potential at a dose of (1/10 LD₅₀) and up-regulated hepatic CYP1A1 mRNA expression in male rats. Additionally, CM supplements may improve the genotoxic outcomes, oxidative stress, and altered CYP1A1 mRNA expression induced by FNP particularly in the pro/concurrent-treatment compared to the concurrent treatment alone.

本研究调查了骆驼奶（CM）在缓解甲型联苯丙菊酯（FNP）II型拟除虫菊酯引起的氧化应激，肝（CYP1A1）mRNA改变中的缓解作用雄性大鼠使用碱性彗星试验（SCGE）的表达模式和DNA损伤。将60只雄性Sprague-Dawley大鼠分为六组（n = 10）：第1个对照组（C），第2个玉米油（CO），第3个（CM）：空腹的CM 2ml /大鼠，第4个（FNP）：空的FNP 7.09 mg / kg体重（BW），第5次（经FNP人工治疗/联合治疗）：首先对CM灌胃15天，然后按相同的剂量和途径对CM + FNP进行灌胃，第六次（FNP + CM联合治疗）：首先对FNP灌胃其次是CM，使用相同的剂量和途径。每天一次，每天两次对大鼠进行口腔灌胃，共60天。FNP暴露可显着降低血清谷胱甘肽（GSH）水平，但可显着提高血清超氧化物歧化酶（SOD），过氧化氢酶（CAT），丙二醛（MDA），羰基蛋白（PCO）和8羟基2脱氧鸟苷（8OH2dG）。另外，暴露于雄性大鼠的全血，肝和脾组织中肝CYP1A1 mRNA表达水平和SCGE指数升高。与（FNP + CM联合治疗）组相比，CM的给药显着调节FNP诱导的氧化应激，降低肝CYP1A1 mRNA表达水平和彗星试验指数值，特别是在（CM + FNP联合/联合治疗）组中。总之，我们的结果首次表明，FNP在（1/10 LD ₅₀）剂量下具有体内遗传毒性潜力，并且在雄性大鼠中肝脏CYP1A1 mRNA表达上调。此外，CM补充剂可能会改善遗传毒性结果，氧化应激和改变CYP1A1 mRNA 与单独同时进行的治疗相比，FNP诱导的表达特别是在前/同时治疗中。