Introduction Inorganic arsenic InAs species

Introduction Inorganic arsenic (InAs) species such as arsenite (AsIII) and arsenate (AsV) are present in groundwater. Arsenic contaminated drinking water is a global public health issue because of its natural prevalence and toxicity. Long exposure to arsenic results in chronic effect in humans, including cancer (skin, lungs and gladder) and non-cancer (hyperpigmentation, keratosis, cardiovascular disease and diabetes) (Quiñones et al., 2006; Sun et al., 2014). Inorganic arsenic species are carcinogens to human classifieds in the Group I (IARC, 2004). The World Health Organization (WHO, 2011) and the US Environmental Protection Agency (US EPA, 2001) recommended a guideline value for arsenic in drinking water as safe level of 10 μg/L. Human exposure to high As concentrations in drinking water above 50 μg/L has been reported in countries like Bangladesh, China and Taiwan. In contrast, reports in Latin America have shown low to moderate concentrations (Caceres et al., 2005; Engström et al., 2007; Bundschuh et al., 2012). Although the distribution of As in soils, sediments, vegetables and irrigation water in Colombia has been recently reviewed (Alonso et al., 2014), there are little data on the As concentrations in groundwater. It must also be noted that there are no available reports of As concentration in groundwater used for drinking water in Colombia. However, guideline for Colombian mandatory regulation is less than 10 μg/L. The metabolic pathway of arsenic in the human body is a complex process which involves a series of steps such as reduction and oxidative methylation. Inorganic arsenic (InAs) is quickly absorbed as arsenite (AsIII) or arsenate (AsV) from the gastrointestinal tract of human and animals. The InAs species are methylated to pentavant species of monomethylarsonic NKY 80 (MMA) and dimethylarsinic acid (DMA). MMA and DMA metabolites are less toxic than InAs species and more readily excrete in urine (Vahter, 2002; Tseng, 2007). However, methylated trivalent species, monomethylarsonous acid (MMAIII) and dimethylarsinous acid (DMAIII) produced as intermediate in the metabolic processing of InAs may be responsible of carcinogenic effects (Yamanaka et al., 2004). Percentages of urinary arsenic species of human exposure reported are 10–30%, 10–20%, and 60–80% for InAs (AsIII and AsV), MMA and DMA, respectively (Hsueh et al., 2002). However, this profile of urinary arsenic speciation (PUAS) can vary largely among individual and population. Several factors have been identified including ethnicity, age, sex, pregnancy, smoking, dietary, frequency and duration of environmental arsenic exposure, and genetic polymorphisms (Agusa et al., 2012; Lovreglio et al., 2012). PUAS are used to assess the individual methylation capacity. Excretion ratios of MMA/InAs and DMA/MMA in the urine are the primary methylation index (PMI) and secondary methylated index (SMI) respectively, which have been proposed as surrogate biomarkers of the arsenic metabolic capacity (Tseng, 2009). Three genes are involved to encode arsenic metabolism: purine nucleoside phosphorylase (PNP), arsenic methyltransferase (AS3MT), and glutathione-S-transferase (GST) (Antonelli et al., 2014). PNP gene has been proposed as a reducing agent from AsV to AsIII (Yu et al., 2003). AS3MT gene is recognized for its importance to methylate AsIII in the species MMAIII and DMAIII (Wood et al., 2006). Recently four members from the GST family including GSTO, GSTP1, GSTT1-null, and GSTM1-null were reported as polymorphic variants that could influence the capacities to metabolize As. GSTO gene (ω class) encodes reducing action from MMAV to MMAIII (Janasik et al., 2015). GSTP1 gene (π class) possibly decreases the activity of GST, generating effects on excretion of DMA (Agusa et al., 2010). Also, the GSTT1-null (θ class) and GSTM1-null (μ class) deletions have been associated with As metabolism mainly to product MMA (Marcos et al., 2006; Zhong et al., 2006). Although the mechanisms are still unclear and the outcome inconsistent, GST gene encodes for a series of phase II enzymes that detoxify xenobiotic via a conjunction reaction with glutathione (GSH).