Long-term chronic food-derived arsenic exposure induce the urinary system metabolic dysfunction in mice.

Arsenic occurs naturally in the environment and humans can be exposed through food, drinking water and inhalation of air-borne particles. Arsenic exposure is associated with cardiovascular, pulmonary, renal, immunologic, and developmental toxicities as well as carcinogenesis. Arsenic displays dose-depen toxicities in target organs or tissues with elevated levels of arsenic. Zinc is an essential micronutrient with proposed protective benefits due to its antioxidant properties, integration into zinc-containing proteins and zinc-related immune signaling. In this study, we tested levels of arsenic and zinc in plasma, kidney, liver, and spleen as model tissues after chronic (42-day) treatment with either arsenite, zinc, or in combination. Arsenite exposure had minimal impact on tissue zinc levels with the exception of the kidney. Conversely, zinc supplementation of arsenite-exposed mice reduced the amount of arsenic detected in all tissues tested. Expression of transporters associated with zinc or arsenic influx and efflux were evaluated under each treatment condition. Significant effects of arsenite exposure on zinc transporter expression displayed tissue selectivity for liver and kidney, and was restricted to Zip10 and Zip14, respectively. Arsenite also interacted with zinc co-exposure for Zip10 expression in liver tissue. Pairwise comparisons show neither arsenite nor zinc supplementation alone significantly altered expression of transporters utilized by arsenic. However, significant interactions between arsenite and zinc were evident for Aqp7 and Mrp1 in a tissue selective manner. These findings illustrate interactions between arsenite and zinc leading to changes in tissue metal level and suggest a potential mechanism by which zinc may offer protection from arsenic toxicities. 

Zinc supplementation alters tissue distribution of arsenic in Mus musculus.

The arsenic (As) release from sediments in great lakes is affected by various factors. In this study, the characteristics of As release from sediments was investigated, and the As sources and sinks with the strengths in sediments from different areas (grass-type, algae-type, and grass-algae alternation areas) in great shallow lakes (Taihu Lake, China) were analyzed, and the influence of P competition in the process of As release was also studied. The results showed that changing trend of the values of equilibrium As concentration in sediments were consistent with the regional changes (0 to 28.12 µg·L−1), and the sediments from algae-type areas had the higher values. The sediments from western lake and northwest lake bay were a strong As and a weak P source, and the north lake bay had the opposite trend of these two regions. Intense P source competition with As from the sediments occurred in algae-type areas. The grass-type areas had strong As and P retention capacities, indicating a sink role of sediment with high As and P sorption capacities. The degree of As and P saturation had similar trend in sediments, and the grass-type areas had the higher values, 18.3%-21.4% and 15.31%-20.34%, respectively. Contribution analysis results showed that most of As release contribution was from the bottom (30-50 cm) sediments, and the surface (0-10 cm) sediments from algae-type areas contributed more to the overlying water than other region. 

Release characteristics of arsenic from sediments and its source or sink competition with phosphorus: A case of a great lake with grass-algae alternation

Rice consumption are a major cause of long-term exposure to arsenic. However, the exact mechanism of the neurotoxic action caused by arsenic exposure remain elusive. The purpose of this study was to investigate the effects of arsenic exposure on the behavior and neuronal structure of Caenorhabditis elegans, followed by the establishment of a 14-month mice model to simulate long-term effects. To elucidate the toxic effects of arsenic on brain metabolism, comprehensive analyses of neurotransmitter content and brain metabolomics were conducted. The findings demonstrated that arsenic exposure led to behavioral impairment, reduced levels of glutamatergic, GABAergic, dopaminergic and serotonergic neurotransmitters, as well as structural abnormalities. The majority of amino acid and fatty acid compounds were found to be upregulated in the hippocampus and cortical tissues. Respectively, an increase in nucleic acid and hydroxy acid-related compounds was observed in hippocampal tissues, while an upregulation of purine ribose-related compounds was detected in cortical tissues. The identified differential metabolites were primarily impacted by glutathione metabolism, arginine and proline metabolism, as well as alanine, aspartate, and glutamate metabolism. Correlation analysis of the hippocampus and cortex yielded compelling evidence of a strong association between glutamate and the majority of the presented metabolites. 

Neurotoxicity and brain metabolic dysfunction induced by long-term food-derived arsenic exposure

Collaborating iron and manganese for enhancing stability of natural arsenic sinks in groundwater: Current knowledge and future perspectives

The exposure and harm of arsenic have attracted wide attention. Rice is an arsenic-rich crop. The purpose of this study was to learn the distribution of arsenic species and the pathological changes in tissues of mice exposed to arsenic-supplemented food simulating rice. Test groups of mice were orally exposed with prepared arsenic feeds supplemented with four arsenic species (arsenite iAsIII, arsenate iAsV, monomethylarsonate MMA, and dimethylarsinate DMA) at three doses (total As concentration: 0.91, 9.1 and 30 μg/g), which simulated the arsenic species ratio in rice. After 112 days, the concentrations of the arsenic species in the spleen, thymus, heart, skin and hair were detected, and histopathology of the spleen, heart and skin was observed. Each arsenic species was detected and their total concentration increased in a dose-dependent manner with a few exceptions. One interesting phenomenon is that ratio of the organic arsenic to inorganic arsenic also increased in a dose-dependent manner. For the other, the order of tissues from high to low arsenic concentration was the same in the medium- and high-dose groups. The histopathological sections of the spleen, heart and skin showed dose-dependent debilitating alterations in tissue architecture. Hyperplasia, hyaline degeneration and sclerosis of fibrous connective tissue occurred in the spleen. Myocardial cell atrophy and interstitial edema occurred in the heart. Hyperpigmentation, hyperkeratosis and atypia of basal cells occurred in the skin. In summary, the long-term intake of high arsenic rice has a health risk. Further studies are needed to assess it.

Distribution of arsenic species and pathological characteristics of tissues of the mice fed with arsenic-supplemented food simulating rice

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Distribution of arsenic species and pathological characteristics of tissues of the mice fed with arsenic-supplemented food simulating rice