## 4 Discussion
These statements are speculative only, because the CBZ effect was not statistically proven, but it opens a space for further investigation to elucidate these potential interactions. Previous studies on high As exposure dose effects have linked As accumulation to disease conditions such as metabolic disorders, nervous and cardiovascular system damage, and malignant transformation in the skin, lungs, liver, and bladder [67; 68]. [PERSON] et al. [66] observed through histopathological examinations that in the organs of mice exposed to a very high arsenic dose, the degree of damage correlated with the increase in As concentration in these organs. Therefore, in this research work, even though histopathological examinations were not conducted on the organs of mice exposed to very high As doses, we anticipate that any potential organ damage due to such exposure will be exacerbated in those of the As + CBZ group compared to the As group. Arsenic, as a redox-sensitive element, is present primarily in soils as As(V) in aerobic conditions, while it is predominantly present as As(III) under anaerobic conditions. It is also known that the presence of As in organic forms is mainly DMA(V) and MMA(V) in the soils [69; 70]. In the scientific literature, the cellular intake of different As species is known to be facilitated by phosphate transporters, aqualylyceroprins, facilitative glucose transporters, and organic anion-transporting polypeptides [71]. From the data of the current research, CBZ's potential influence on enhanced intake of As only occurred at very high As doses. However, the mechanisms of this pharmaceutical on any of these cellular As transporters to enhance As intake were not investigated in this study and are subject to future research. In the present study, in all the experimental animal groups, the order of total As concentrations in the organs was as follows: kidney > liver > spleen > lungs. Identifying specific As target organs is crucial for understanding the mode of action of As-influenced toxicity and carcinogenicity [63]. The findings of this study indicated that the kidney, the liver, and the spleen were the major target organs for As distribution and concentration after absorption, while minor distributions and concentrations were observed in the lungs. In that regard, [PERSON] et al. [63] and [PERSON] et al. [72] observed the kidney as the predominant target organ after As absorption and distribution in mice. This is due to arsenate (which possesses similar physicochemical features as phosphate) reabsorption by phosphate transporters in the renal proximal tubules [63]. The liver is a target organ since it is the major site where the As methylation process occurs [73; 74]. [PERSON] and [PERSON] [75] observed that the spleen was the organ that accumulated the most As in rats. According to [PERSON] and [PERSON] [75] and [PERSON] et al. [76], the presence of 'white lymphocyte-enriched pulp' and'red erythrocyte-enriched pulp with macrophages' in the spleen are potential As accumulation target sites. Contrary to the findings of this study, which documented minor concentrations of As in the lungs, previous research works have indicated the human lungs as a major target for As concentration [77; 78]. According to [PERSON] et al. [72], [PERSON] et al. [73], [PERSON] et al. [65], and [PERSON] et al. [79], the pattern of As distribution and accumulation in organs in mammals may vary significantly due to exposure duration, the applied protocol of dose administration, species of the animal, and the presence of GSH and other thiol (-SH)-containing groups. In this study, we assessed As species' methylation (metabolism) and their concentrations in the experimental animal groups solely in the liver. The liver was chosen because it is known to be the major site where inorganic As methylation occurs when As is administered orally [59; 74]. Four identifiable quantities of As species were measured in the liver of all the experimental animal groups, comprising As(III), As(V), DMA, and MMA.