We can't find the internet
Attempting to reconnect
Something went wrong!
Hang in there while we get back on track
Fasn involved in the nephrotoxicity induced by polystyrene nanoplastics and the intervention of melatonin through intestinal microbiota-mediated lipid metabolism disorder
AI summary Read the abstract
In mice, polystyrene nanoplastics impaired kidney function, and the damage was linked to lipid metabolism changes driven by gut bacteria. The authors trace a pathway from Desulfovibrionales bacteria through the gene Fasn to the fatty acid DHA. Mice given melatonin had less kidney toxicity and altered Fasn expression.
Nanoplastics (NPs) can accumulate in the kidney and cause kidney injury, but the multi-organ interaction mechanism and preventive measures of kidney injury are still unclear. In this study, in vivo (60 µg/day, 42 days) and in vitro (0.4 µg/µL, 24 h) exposure models of polystyrene nanoplastics (PS-NPs, 80 nm) in mice and human kidney cortex proximal tubule epithelial cells (HK-2 cells) were established, respectively. Our study revealed that PS-NPs caused obvious pathological changes and impaired renal function in mice, which were related to lipid metabolism disorders mediated by intestinal flora. Desulfovibrionales-fatty acid synthase (Fasn)-docosahexaenoic acid (DHA) pathway may be one of the mechanisms of kidney injury in mice. Importantly, we also found that melatonin attenuates PS-NPs-induced nephrotoxicity by modulating lipid metabolism disorders (represented by DHA) and affects Fasn expression. In conclusion, our study revealed the important role of intestinal flora-mediated lipid metabolism in PS-NPs-induced nephrotoxicity and preliminarily provided potential key gene targets and effective preventive measures for PS-NPs-induced nephrotoxicity.
More Papers Like This
Exploring the Mechanismof Kidney Injury in Mice Inducedby High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Throughthe Kidney-Gut Axis
AI summary Read the abstract
This mouse study found that combining a high-fat diet with polystyrene nanoplastic exposure (100 nm, 25 mg/kg/day) worsened kidney toxicity beyond high-fat diet alone, with the combination disrupting lipid metabolism via tryptophan and glycerophospholipid pathways and exacerbating gut microbiota dysbiosis through the kidney-gut axis.
Investigation of nephrotoxicity on mice exposed to polystyrene nanoplastics and the potential amelioration effects of DHA-enriched phosphatidylserine
AI summary Read the abstract
In mice, 100 nanometer polystyrene nanoplastics caused kidney toxicity through inflammation, oxidative stress and disturbed lipid metabolism. Mice given DHA-enriched phosphatidylserine had lower inflammatory markers and higher antioxidant enzyme activity in the kidney. The authors report this as the first study of the compound in this model.
Melatonin and probiotics ameliorate nanoplastics-induced hematopoietic injury by modulating the gut microbiota-metabolism
AI summary Read the abstract
Researchers found that melatonin and probiotics can ameliorate nanoplastic-induced hematopoietic injury in mice by modulating gut microbiota and metabolism, offering potential prevention strategies against plastic particle toxicity to bone marrow stem cells.
Melatonin prevents the transgenerational toxicity of nanoplastics in zebrafish (Danio rerio)
AI summary Read the abstract
Adult zebrafish were exposed to polystyrene nanoplastics for 14 days, with or without melatonin, and their embryos were studied. Parental exposure at 1 mg/L lowered fertilization and survival rates in the offspring and raised deformity rates and oxidative stress. Offspring of fish that also received melatonin showed fewer of these effects.
Exploring the Mechanism of Kidney Injury in Mice Induced by High-Fat Diet and Polystyrene Nanoplastics Co-Exposure Through the Kidney-Gut Axis
AI summary Read the abstract
In a mouse study, the combination of a high-fat diet and polystyrene nanoplastics caused worse kidney damage than either exposure alone, working through the kidney-gut connection. The nanoplastics plus high-fat diet disrupted gut bacteria, increased inflammation, and triggered a harmful immune response that traveled from the gut to the kidneys. This suggests that people who eat high-fat diets may be more vulnerable to kidney damage from nanoplastic exposure.
Research digests by email
When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.