Arsenic is a public concern due to its widespread occurrence and carcinogenicity. Consumption of arsenic-contaminated fish is an important exposure pathway for human health. This study focused on understanding how exposure to arsenic-contaminated fish is informative to human health risk assessment. While the bioaccumulation and tissue distributions of total arsenic concentration in fish are commonly reported, there are limited studies related to the time-course of arsenic species in various tissues. Using the Tilapia as a case, this study aimed to investigate the bioaccumulation and tissue distributions (liver, gastrointestinal (GI), muscle, and gill) of arsenic species in freshwater fish via diet-borne inorganic arsenic exposure. In particular, the Tilapia were exposed to arsenic (III) and As(V) for 32 days. The accumulation of arsenic in all tissues linearly increased with time in the first 10 days’ exposure, while the arsenic levels remained stable in the following 20 days’ exposure. The accumulation of arsenic in tissue followed the sequence of intestine > liver > gill > muscle. Meanwhile, more than 90% of arsenic was converted into organic form in liver, gill, and muscle, while organic arsenic contributed about 30–80% to the total arsenic in the GI. The percentage of organic form in muscle is the highest, followed by gill, liver, and intestine, and arsenobetaine is the main form of organic arsenic. While the exposure profiles of As(III) and As(V) are quite similar, the absorption rate of As(V) is relatively higher than that of As(III). Information provided here can be instrumental for exposure assessment and risk management for arsenic in aquatic environment.

Exploring how risk genes cumulatively impair brain function in preclinical phase (i.e., in cognitively normal elderly) could provide critical insights into the pathophysiology of Alzheimer's disease (AD). Working memory impairment has always been a considerable cognitive deficit in AD, which is likely under complex genetic control. Though, the APOE ɛ4 allele could damage the working memory performance in normal elderly, dissociable results have been reported. This allele may exert specific effects in contexts with other genetic variants. The rs2618516 in the spondin 1 gene (SPON1) has been associated with AD risk and brain structure in the elderly. SPON1 may interact with APOE through processing the amyloid precursor protein and suppressing amyloid-β levels. Using neuropsychological tasks from 710 individuals, we found significant SPON1 × APOE genotype interactions in working memory and executive function performances. Moreover, such interaction was also found in regional brain activations based on functional magnetic resonance imaging data with the n-back working memory task performed in a sub-cohort of 64 subjects. The effects of ɛ4 allele on activation of right inferior frontal gyrus, triangular part (IFGtriang.R) were modulated by rs2618516 in a working memory task. Furthermore, lower IFGtriang.R activation was associated with better cognitive functions. Moreover, the IFGtriang.R activation could mediate the impacts of SPON1 × APOE interactions on working memory performance. These findings suggested the importance of weighing APOE effects on brain activation under the working memory task within the context of the SPON1 genotype.

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