Faculty of Medicine, Training Hospital, Van Yuzuncu Yil University, Van, Turkey.
Faculty of Veterinary Medicine, Biochemistry Department, Van Yuzuncu Yil University, Van, Turkey.
Biol Trace Elem Res. 2021 Jan;199(1):136-141. doi: 10.1007/s12011-020-02121-y. Epub 2020 Apr 10.
This study was planned to determine the molecular basis and causes of damage to the kidney and the liver, which are the most affected tissues in sheep exposed to chronic fluoride. For this purpose, liver and kidney tissues were obtained from sheep with signs of fluorosis in the age range of 4-6 years. The control group consisted of clinically healthy sheep without fluorosis. The apoptotic and oxidative genes expression of target genes was determined using the real qRT-PCR method. According to the control gene (Gapdh) that was detected that in the liver, the apoptotic genes caspase-8, caspase-9, and Bim increased and caspase-3, Bcl-2, and Bak decreased, while in the kidney, caspase-3 and Bax and caspase-8, Bcl-2, Bcl2l-1, Bim, and Bak decreased. According to the 2-ΔCt values of the oxidative stress genes, it was determined that Cygb, Gstp1, and Ncf1 genes increased significantly in the fluorosis group and Gpx1, sod1, and sod2 genes decreased significantly. In the kidney tissue, Cygb and Gpx1 increased in the fluorosis group, while sod1, sod2, Gstp1, Ncf1 and Ccs, and Nos2 were found to decrease significantly. As a result, it was shown that apoptosis and oxidative mechanisms are activated in the liver and the kidney tissues of sheep with fluorosis and these parameters have an important role in understanding the molecular basis of tissue damage in fluorosis.
本研究旨在确定慢性氟暴露的绵羊中受影响最严重的组织——肾脏和肝脏损伤的分子基础和原因。为此,从 4-6 岁具有氟中毒迹象的绵羊中获取肝脏和肾脏组织。对照组由无氟中毒临床症状的健康绵羊组成。使用实时 qRT-PCR 方法确定目标基因的凋亡和氧化基因表达。根据在肝脏中检测到的对照基因(Gapdh),凋亡基因 caspase-8、caspase-9 和 Bim 增加,而 caspase-3、Bcl-2 和 Bak 减少,而在肾脏中,caspase-3 和 Bax 和 caspase-8、Bcl-2、Bcl2l-1、Bim 和 Bak 减少。根据氧化应激基因的 2-ΔCt 值,确定在氟中毒组中 Cygb、Gstp1 和 Ncf1 基因显著增加,而 Gpx1、sod1 和 sod2 基因显著减少。在肾脏组织中,氟中毒组中 Cygb 和 Gpx1 增加,而 sod1、sod2、Gstp1、Ncf1 和 Ccs 以及 Nos2 显著减少。结果表明,凋亡和氧化机制在氟中毒绵羊的肝脏和肾脏组织中被激活,这些参数对于理解氟中毒组织损伤的分子基础具有重要作用。