Phosphate Uptake and Its Relation to Arsenic Toxicity in Lactobacilli.

The use of probiotic lactobacilli has been proposed as a strategy to mitigate damage associated with exposure to toxic metals. Their protective effect against cationic metal ions, such as those of mercury or lead, is believed to stem from their chelating and accumulating potential. However, their retention of anionic toxic metalloids, such as inorganic arsenic, is generally low. Through the construction of mutants in phosphate transporter genes (pst) in Lactiplantibacillus plantarum and Lacticaseibacillus paracasei strains, coupled with arsenate [As(V)] uptake and toxicity assays, we determined that the incorporation of As(V), which structurally resembles phosphate, is likely facilitated by phosphate transporters. Surprisingly, inactivation in Lc. paracasei of PhoP, the transcriptional regulator of the two-component system PhoPR, a signal transducer involved in phosphate sensing, led to an increased resistance to arsenite [As(III)]. In comparison to the wild type, the phoP strain exhibited no differences in the ability to retain As(III), and there were no observed changes in the oxidation of As(III) to the less toxic As(V). These results reinforce the idea that specific transport, and not unspecific cell retention, plays a role in As(V) biosorption by lactobacilli, while they reveal an unexpected phenotype for the lack of the pleiotropic regulator PhoP.

Impact of Chronic Exposure to Arsenate through Drinking Water on the Intestinal Barrier.

Chronic exposure to inorganic arsenic (As) [As(III) + As(V)], which affects millions of people, increases the incidence of some kinds of cancer and other noncarcinogenic pathologies. Although the oral pathway is the main source of exposure, in vivo studies conducted to verify the intestinal toxicity of this metalloid are scarce and are mainly focused on evaluating the toxicity of As(III). The aim of this study was to evaluate the effect of chronic exposure (6 months) of BALB/c mice to As(V) (15-60 mg/L) via drinking water on the different components of the intestinal barrier and to determine the possible mechanisms involved. The results show that chronic exposure to As(V) generates a situation of oxidative stress (increased lipid peroxidation and reactive species) and inflammation (increased contents of several proinflammatory cytokines and neutrophil infiltrations) in the intestinal tissues. There is also evidence of an altered expression of constituent proteins of the intercellular junctions (Cldn1, Cldn3, and Ocln) and the mucus layer (Muc2) and changes in the composition of the gut microbiota and the metabolism of short-chain fatty acids. All of these toxic effects eventually may lead to the disruption of the intestinal barrier, which shows an increased paracellular permeability. Moreover, signs of endotoxemia are observed in the serum of As(V)-treated animals (increases in lipopolysaccharide-binding protein LBP and the proinflammatory cytokine IL-1ß). The data obtained suggest that chronic exposure to As(V) via drinking water affects the intestinal environment.

Dietary microplastics: Occurrence, exposure and health implications.

The increasing use of plastic materials generates an enormous amount of waste. In the aquatic environment, a significant part of this waste is present in the form of microplastics (MPs)- particles with a diameter of between 0.1 µm and 5 mm. The arrival of these small plastics in the food chain has been recently documented. MPs have been reported in fishery products, drinking water and sea salt among other foods. Their intestinal absorption is considered limited due to their size, however, they contain a mixture of chemicals intentionally added during their manufacture, which could cross the intestinal barrier. Currently there are not enough data to allow an accurate assessment of the risk associated with dietary exposure to MPs. The lack of robust methodologies is undoubtedly one of the main problems. There is limited information on occurrence in dietary sources (drinking water and food), human intake, toxicokinetics and long term toxicity of these contaminants. The present review describes the studies published so far and points to the need for improved knowledge in order to have a more accurate view of the problems posed by MPs.

Arsenic in Tissues and Prey Species of the Scalloped Hammerhead (Sphyrna lewini) from the SE Gulf of California.

The bioaccumulation of arsenic (As) in the muscle, liver, kidneys, and brain of the shark Sphyrna lewini was measured in 40 juvenile specimens from southeast Gulf of California. Additionally, the biomagnification factor was calculated through prey items from stomach contents of the analyzed specimens. The concentrations of As (mg kg-1, wet weight) were higher in the muscle (10.1 ± 0.3) and liver (9.4 ± 0.5) than in the brain (4.5 ± 0.3) and kidneys (4.2 ± 0.2), which may be attributed to the biological functions of each tissue. Positive correlations were found between the levels of As in muscle and liver with the biological parameters of S. lewini. Hammerhead sharks feed mainly of teleost fishes with low As values (Clupeidae fishes, 1.1 ± 0.5; Sciaenidae fishes, 1.0 ± 0.6; Scomber japonicus, 1.2 ± 0.6; and Etropus crossotus 2.1 ± 0.4) compared with the predator, indicating biomagnification. Inorganic arsenic (Asi) in muscle was estimated as 3% of the total As, although muscle consumption is unlikely to represent a risk (HQ < 1) in humans. Moreover, the probabilities of developing cancer were estimated as low (3.99 × 10-5 to 3.32 × 10-6). To avoid health risks related to As, a weekly ration must not exceed 69.3 and 484.8 g in children and adults, respectively.

Use of lactic acid bacteria and yeasts to reduce exposure to chemical food contaminants and toxicity.

Chemical contaminants that are present in food pose a health problem and their levels are controlled by national and international food safety organizations. Despite increasing regulation, foods that exceed legal limits reach the market. In Europe, the number of notifications of chemical contamination due to pesticide residues, mycotoxins and metals is particularly high. Moreover, in many parts of the world, drinking water contains high levels of chemical contaminants owing to geogenic or anthropogenic causes. Elimination of chemical contaminants from water and especially from food is quite complex. Drastic treatments are usually required, which can modify the food matrix or involve changes in the forms of cultivation and production of the food products. These modifications often make these treatments unfeasible. In recent years, efforts have been made to develop strategies based on the use of components of natural origin to reduce the quantity of contaminants in foods and drinking water, and to reduce the quantity that reaches the bloodstream after ingestion, and thus, their toxicity. This review provides a summary of the existing literature on strategies based on the use of lactic acid bacteria or yeasts belonging to the genus Saccharomyces that are employed in food industry or for dietary purposes.

In vivo evaluation of the effect of arsenite on the intestinal epithelium and associated microbiota in mice.

Chronic exposure to inorganic arsenic (As) [As(III) + As(V)], which affects millions of people, increases the incidence of some kinds of cancer and other non-carcinogenic pathologies. Although the oral pathway is the main form of exposure, in vivo studies have not been conducted to verify the intestinal toxicity of this metalloid. The aim of this study is to perform an in vivo evaluation of the intestinal toxicity of inorganic As, using female BALB/c mice exposed through drinking water to various concentrations of As(III) (20, 50, and 80 mg/L) for 2 months. An increase was observed in oxygen and/or nitrogen reactive species, and in gene and protein expression of pro-inflammatory cytokines (IL-1ß, IL-2, IL-6) at concentrations equal to or greater than 50 mg/L. These changes were accompanied by a profound remodeling of the intestinal microbial profile in terms of diversity and global composition, which could be at the basis or exacerbate As(III) toxic effects. The histological study showed that there was moderate inflammation of the mucosa and submucosa, accompanied by hyperplasia of crypts at the highest administered dose. In addition, all the treatments with As(III) resulted in a decreased expression of Muc2, which encodes one of the main components of the intestinal layer of mucus. The effects described are compatible with the increased intestinal permeability observed at concentrations equal to or greater than 50 mg/L, indicative of loss of barrier function.

Effect of chronic exposure to inorganic arsenic on intestinal cells.

Chronic exposure to inorganic arsenic (As)-As(III) + As(V)-is associated with type 2 diabetes, vascular diseases and various types of cancer. Although the oral route is the main way of exposure to inorganic As, the adverse gastrointestinal effects produced by chronic exposure are not well documented. The aim of the present study is to evaluate the effect of chronic exposure to As(III) on the intestinal epithelium. For this purpose, NCM460 cells, non-transformed epithelial cells from the human colon, were exposed to As(III) (0.01-0.2 mg/L) for 6 months and monitored for acquisition of a tumor-like phenotype. Secretion of matrix metalloproteinases, histone modifications (H3 acetylation), hyperproliferation capacity, formation of floating spheres, anchorage-independent growth, release of cytokine interleukin-8 and expression of relevant genes in colon tumorigenesis were assessed. The results show a maintained proinflammatory response from the beginning, with an increase in interleukin-8 secretion (≤570%). Downregulation of CDX1 and CDX2 was also observed. After 14 weeks of exposure, cells presented marked increases in matrix metalloproteinase-2 secretion and histone modifications. As(III)-treated cells were hyperproliferative, grew in low-serum media and were able to form free-floating spheres. Overall, these data suggest that exposure of human colon epithelial cells to As(III) facilitates acquisition of transformed cell characteristics.

Dietary compounds as modulators of metals and metalloids toxicity.

A large part of the population is exposed to metals and metalloids through the diet. Most of the in vivo studies on its toxicokinetics and toxicity are conducted by means of exposure through drinking water or by intragastric or intraperitoneal administration of aqueous standards, and therefore they do not consider the effect of the food matrix on the exposure. Numerous studies show that some components of the diet can modulate the toxicity of these food contaminants, reducing their effect on a systemic level. Part of this protective role may be due to a reduction of intestinal absorption and subsequent tissue accumulation of the toxic element, although it may also be a consequence of their ability to counteract the toxicity directly by their antioxidant and/or anti-inflammatory activity, among other factors. The present review provides a compilation of existing information about the effect that certain components of the diet have on the toxicokinetics and toxicity of the metals and metalloids of greatest toxicological importance that are present in food (arsenic, cadmium, lead, and mercury), and of their most toxic chemical species.

Metal(loid) contamination in seafood products.

Seafood products are important sources of proteins, polyunsaturated lipids and phospholipids, and also of numerous micronutrients (vitamins and minerals). However, they may also present chemical contaminants that can constitute a health risk and that must be considered when evaluating the risk/benefit associated with consumption of this group of foods. Toxic metals and metalloids in seafood, such as mercury (Hg), cadmium (Cd), arsenic (As), and lead (Pb), are subjected to legislative control in order to provide the consumer with safe seafood. This review provides an exhaustive survey of the occurrence of these toxic metal(loid)s in seafood products, and of the risk resulting from their consumption. Consideration is given to aspects related to speciation, food processing, and bioavailability, which are key factors in evaluating the risk associated with the presence of these toxic trace elements in seafood products.

Characterization of the binding capacity of mercurial species in Lactobacillus strains.

BACKGROUND: Metal sequestration by bacteria has been proposed as a strategy to counteract metal contamination in foodstuffs. Lactobacilli can interact with metals, although studies with important foodborne metals such as inorganic [Hg(II)] or organic (CH3 Hg) mercury are lacking. Lactobacilli were evaluated for their potential to bind these contaminants and the nature of the interaction was assessed by the use of metal competitors, chemical and enzymatical treatments, and mutants affected in the cell wall structure. RESULTS: Lactobacillus strains efficiently bound Hg(II) and CH3 Hg. Mercury binding by Lactobacillus casei BL23 was independent of cell viability. In BL23, both forms of mercury were cell wall bound. Their interaction was not inhibited by cations and it was resistant to chelating agents and protein digestion. Lactobacillus casei mutants affected in genes involved in the modulation of the negative charge of the cell wall anionic polymer lipoteichoic acid showed increased mercury biosorption. In these mutants, mercury toxicity was enhanced compared to wild-type bacteria. These data suggest that lipoteichoic acid itself or the physicochemical characteristics that it confers to the cell wall play a major role in mercury complexation. CONCLUSION: This is the first example of the biosorption of Hg(II) and CH3 Hg in lactobacilli and it represents a first step towards their possible use as agents for diminishing mercury bioaccessibility from food at the gastrointestinal tract. © 2017 Society of Chemical Industry.