RESUMO
Massive amounts of microplastics are transported daily from the oceans and rivers onto beaches. The ocean plastisphere is a hotspot and a vector for antibiotic resistance genes (ARGs) and potentially pathogenic bacteria. However, very little is known about the plastisphere in beach sand. Thus, to describe whether the microplastics from beach sand represent a risk to human health, we evaluated the bacteriome and abundance of ARGs on microplastic and sand sampled at the drift line and supralittoral zones of four beaches of poor and good water quality. The bacteriome was evaluated by sequencing of 16S rRNA gene, and the ARGs and bacterial abundances were evaluated by high-throughput real-time PCR. The results revealed that the microplastic harbored a bacterial community that is more abundant and distinct from that of beach sand, as well as a greater abundance of potential human and marine pathogens, especially the microplastics deposited closer to seawater. Microplastics also harbored a greater number and abundance of ARGs. All antibiotic classes evaluated were found in the microplastic samples, but not in the beach sand ones. Additionally, 16 ARGs were found on the microplastic alone, including genes related to multidrug resistance (blaKPC, blaCTX-M, tetM, mdtE and acrB_1), genes that have the potential to rapidly and horizontally spread (blaKPC, blaCTX-M, and tetM), and the gene that confers resistance to antibiotics that are typically regarded as the ultimate line of defense against severe multi-resistant bacterial infections (blaKPC). Lastly, microplastic harbored a similar bacterial community and ARGs regardless of beach water quality. Our findings suggest that the accumulation of microplastics in beach sand worldwide may constitute a potential threat to human health, even in beaches where the water quality is deemed satisfactory. This phenomenon may facilitate the emergence and dissemination of bacteria that are resistant to multiple drugs.
Assuntos
Microplásticos , Qualidade da Água , Humanos , Plásticos , Areia , Antibacterianos/farmacologia , RNA Ribossômico 16S/genética , Bactérias/genética , Resistência Microbiana a Medicamentos/genética , Genes BacterianosRESUMO
Obesity in fathers leads to DNA damage and epigenetic changes in sperm that may carry potential risk factors for metabolic diseases to the next generation. Taurine (TAU) supplementation has demonstrated benefits against testicular dysfunction and pancreatic islet impairments induced by obesity, but it is not known if these protective actions prevent the propagation of metabolic disruptions to the next generation; as such, we hypothesized that paternal obesity may increase the probability of endocrine pancreatic dysfunction in offspring, and that this could be prevented by TAU supplementation in male progenitors. To test this, male C57Bl/6 mice were fed on a control diet (CTL) or a high-fat diet (HFD) without or with 5% TAU in their drinking water (CTAU and HTAU) for 4 months. Subsequently, all groups of mice were mated with CTL females, and the F1 offspring were identified as: CTL-F1, CTAU-F1, HFD-F1, and HTAU-F1. HFD-fed mice were normoglycemic, but glucose intolerant and their islets hypersecreted insulin. However, at 90 days of age, HFD-F1 offspring displayed normal glucose homeostasis and adiposity, but reduced glucose-induced insulin release. HFD-F1 islets also exhibited ß- and α-cell hypotrophy, and lower δ-cell number per islet. Paternal TAU supplementation prevented the decrease in glucose-induced insulin secretion and normalized ß-cell size and δ-cell number, and increased α-cell size/islet in HTAU-F1 mice. In conclusion, HFD consumption by male founders decreases ß-cell secretion and islet-cell distribution in their offspring. TAU attenuates the deleterious effects of paternal obesity on insulin secretion and islet-cell morphology in F1 offspring.