Effects of microplastics and lead exposure on gut oxidative stress and intestinal inflammation in common carp (Cyprinus carpio L.).

Microplastics (MPs) are increasingly being detected in freshwater environments, which have the potential to cause combined toxicity with other contaminants on aquatic organisms. To reveal the ecological risks, the combined effects of lead (Pb) and polyvinyl chloride microplastics (MPs) were explored in the gut of common carp (Cyprinus carpio L.). The results confirmed that exposure of Pb alone accelerated Pb accumulation, increased oxidative stress, and activated the inflammation response of the gut. However, the aforementioned effects all decreased under the co-exposure of Pb and MPs. In addition, MPs altered intestinal microbial community of common carp, especially the abundance of immune system-related species. All measured variables were organized for partial least square path modeling, which revealed the combined effects of Pb and MPs on inflammation response. The results implied that MPs reduced inflammation response in two ways, including the reduction of intestinal Pb accumulation and the alteration of the intestinal microbial community. Overall, this study provides a novel aspect of ecological effects on aquatic animals from Pb and MPs exposure. The interesting results remind us that when exploring the ecological risks of MPs, combined effects from other toxic substances must be considered simultaneously.

The universality of eAREs in animal feces suggesting that eAREs function possibly in horizontal gene transfer.

Objectives: This study aimed to pinpoint the universality of extracellular antimicrobial resistance elements (eAREs) and compare the contents of eAREs with those of intracellular AREs (iAREs) in animal feces, thus laying a foundation for the further analysis of the horizontal transfer of antimicrobial resistance genes (ARGs) in the animal guts. Materials and Methods: Extracellular DNAs were isolated from the fecal samples of Pavo cristatus (n = 18), Ursus thibetanus (n = 2), two breeds of broilers (n = 21 and 11, respectively), and from the contents of rabbit intestines (n = 5). eAREs were detected by PCR technology. iAREs in P. cristatus and broiler feces were also detected and compared with the corresponding eAREs. In addition, some gene cassettes of class 1 integrons were sequenced and analyzed. Results: The results showed that eAREs exist in animal feces and intestinal contents. In this study, different eAREs were detected from animal feces and intestinal contents, and tetA, tetB, sul1, sul2, class 1 integron, and IncFIB presented the highest detection rates. The detection rates of certain eAREs were significantly higher than those of parallel iAREs. The integral cassettes with intact structures were found in eAREs, and the cassettes carried ARGs. Conclusions: The presented study here sheds light on the presence of eAREs in animal feces or guts, and eAREs may play an important role in the horizontal gene transfer of ARGs.

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study.

BACKGROUND: Pre-administration of probiotic Lactobacilli attenuates ethanol-induced gastric mucosal injury (GMI). The underpinning mechanisms remain to be elucidated. We speculated that lactate, the main metabolite of Lactobacillus that can be safely used as a common food additive, mediated the gastroprotective effect. This study aimed to gain experimental evidence to support our hypothesis and to shed lights on its underlying mechanisms. METHODS: Lactate was orally administrated to mice at different doses 30 min prior to the induction of GMI. Gastric tissue samples were collected and underwent histopathological and immunohistochemical assessments, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction (qPCR) and western blot analyses. RESULTS: Pretreatment with lactate at 1-3 g/kg significantly curtailed the severity of ethanol-induced GMI, as shown by morphological and histopathological examinations of gastric tissue samples. Significantly lower level of cytokines indicative of local inflammation were found in mice receiving lactate treatment prior to ethanol administration. Western-blot, immunohistochemical analysis and qPCR suggested that gastroprotective properties of lactate were mediated by its modulatory effects on the expression of the apoptosis regulator gene Bax, the apoptotic executive protein gene Casp3, and genes critical for gastric mucosal integrity, including those encoding tight junction proteins Occludin, Claudin-1, Claudin-5, and that for lactate receptor GPR81. CONCLUSION: Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.