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    • The iAs mainly metabolized in

    2022-06-22

    The iAs mainly metabolized in the liver to generate MMA and DMA. DMA, MMA and iAs were excreted through the urine (Khaleghian et al., 2014; Wei et al., 2017a). Pearson correlation coefficient was used to explore associations between concentrations of three arsenic species in urine and gene expression. The most interesting finding was that the levels of gene Nicotine were positively correlated with the concentrations of urinary tAs, DMA, MMA and iAs in all subjects. Toxicological studies had indicated that the three different arsenic species exert different roles (Banerjee et al., 2014; Wang et al., 2015). We wanted to know the effect of three arsenic species on Fas and Bax mRNA expression. Gene expression analysis showed that MMA and DMA had no effect on Bax gene mRNA expression and decreased Fas gene mRNA expression in MDA-MB-231 and XWLC-05 cells. Three different arsenic species had different roles in inducing gene expression. We thought this was the reason for the inconsistency between the different studies. Intracellular arsenic metabolism requires SAM as a methyl donor (Khaleghian et al., 2014). Previous studies have shown that the methyl donor, SAM, reduced arsenic trioxide-induced up-regulation of gene mRNA and protein expression (Du et al., 2012). In our study, SAM did not reduce sodium arsenite-induced up-regulation of Fas and Bax mRNA. The iAs can induce cellular apoptosis in leukemia and various forms of solid cancer cells. Apoptosis is a complex process that involves large number of genes expression. Apoptosis is a controlled process of genes, such as Bax/Bcl-2 ratio, Smac (second mitochondria-derived activator of caspases), Fas/fasl and p53. Our date showed that iA increased expression of Bax gene in vivo and vitro, But level of Bcl-2 expression were not examined. Perhaps this was regret. Previous evidence suggested that exposure to iAs increases the expression of p53 protein (Yu et al., 2014; Choudhury et al., 2016). The mechanism responsible for the fact that exposure to iAs result in the activation of p53 functions, which mainly attributed to the increased expression of Fas and Bax gene. Fas and Bax gene were also regulated by some other signaling pathways.
    Disclosure of potential conflicts of interest
    Acknowledgement This work was supported by the projects of Yunnan Natural Science Foundation [2017FB123] and Graduate Science Foundation [2017S005].The authors acknowledge Weihua Weng and Sun Giufan for his technical input.
    Introduction Familial Mediterranean Fever (FMF) is an autosomal recessive hereditary disease. It is characterized by recurrent episodes of fever, abdominal pain, chest pain, erysipelas-like erythema, arthritis and pleurisy attacks (Kastner, 2001, Samuels and Ozen, 2000, Ben-Chetrit and Levy, 1998). Although FMF has been reported to be more prevalent among Turkish, Arab, Jewish and Armenian populations, it is now possible to find disease in various countries of the world due to migration (Samuels et al., 1998, Touitou, 2001). The prevalence of the disease in Turkish population is reported to be 1/10,000 and the carrier ratio is 1/5 (Yilmaz et al., 2001). Fas (APO-1/CD95) is a member of the tumor necrosis factor receptor superfamily. It is a type 1 membrane protein with a molecular weight of 45kDa. It was found to play a central role in the apoptosis signaling of various cells and tissues including neutrophils. (Kischkel et al., 1995, Nagata, 1994, Leithauser et al., 1993, Itoh et al., 1991). The ligand of the Fas receptor (Fas ligand, Fas L) is a 40kDa molecule which is found in the form of dimer or trimer in circulation (Kischkel et al., 1995). Fas-FasL is the primary mediator of apoptosis in many physiological processes (Nagata and Golstein, 1995). The FAS is localized on the short arm of the chromosome 10 and consists of 9 exons and 8 introns. The FASLG is located on the chromosome 1 and consists of 4 exons and 3 introns (Sibley et al., 2003). Single nucleotide polymorphisms in the promoter region of the FAS (G or A at position -1377 [FAS c.-1377GA] and A or G at position -671 [FAS c.-671 AG]) and FASLG (T or C at position -844 [FASLG c.-844C>T]) genes alter the transcriptional activity of the gene (Sun et al., 2004). The Fas-FasL system is an important mechanism in the regulation of apoptosis, and disorders in the Fas-FasL system play an important role in several diseases, including inflammatory diseases (Öktem et al., 2001). In autoimmune diseases, defects in Fas pathway and the increases in Fas levels were reported (Fisher et al., 1995, Cheng et al., 1994). The aim of this study was to investigate whether the FAS c.-671A>G and FASLG c.-844C>T polymorphisms are associated with susceptibility to FMF and their relationships with the main clinical manifestations of the disease.