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Maternal Exposure to Microplastics and High-Fructose Diet Induces Offspring Hypertension via Disruption of H2S Signaling, Gut Microbiota, and Metabolic Networks
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Researchers found that maternal exposure to both microplastics and a high-fructose diet during pregnancy and lactation raised blood pressure in rat offspring, with additive effects when the two exposures were combined. Microplastic exposure suppressed hydrogen sulfide signaling enzymes in the kidneys and altered gut microbial communities linked to blood pressure regulation. The study suggests that prenatal microplastic exposure may program long-term cardiovascular and kidney risks in offspring through disrupted metabolic pathways.
Maternal consumption of a high-fructose (HF) diet or exposure to microplastics (MPs) can each independently affect kidney development and increase the risk of hypertension in adult offspring, yet their combined impact remains poorly understood. Dysregulation of hydrogen sulfide (H2S) signaling and alterations in gut microbiota are potential mediators of this programming. Pregnant rats received either standard chow or a 60% HF diet, with half of each group additionally exposed to sulfate-modified MPs (1 mg/L) with a 5 μm diameter throughout pregnancy and lactation. Male offspring were divided into four groups (n = 7-8 per group): control, HF, MP, and HF+MP. Maternal HF or MP exposure raised offspring blood pressure (BP), with additive effects when combined, and MP exposure caused renal injury. MP treatment also suppressed renal H2S-generating enzymes and reduced H2S production. Both HF and MP exposures altered gut microbial composition linked to BP regulation and induced metabolic changes in taurine/hypotaurine and sulfur pathways, suggesting impaired H2S production. These results indicate that maternal HF and MP exposures interfere with H2S signaling, gut microbiota, and metabolic programming, highlighting the H2S signaling as a potential target to reduce long-term kidney and cardiometabolic risks.
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Researchers used a two-hit model in rats to examine whether maternal microplastic exposure during pregnancy and nursing worsens the effects of direct microplastic exposure later in life. They found that combined maternal and postnatal exposure elevated blood pressure more than either exposure alone, with effects linked to oxidative stress and changes in gut bacteria. The study suggests that microplastic exposure may have compounding effects across generations, raising concerns about long-term cardiovascular and kidney health.
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Researchers found that people with high blood pressure had more microplastics in their stool samples than healthy individuals, and feeding microplastics to mice raised their blood pressure and caused heart damage. The harm was linked to changes in gut bacteria, and a high-fiber diet or antibiotics helped reduce the damage. This study suggests microplastic exposure may worsen heart and blood pressure problems by disrupting the gut microbiome.
Prenatal High-Fat Diet Combined with Microplastic Exposure Induces Liver Injury via Oxidative Stress in Male Pups
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Researchers studied the combined effects of a maternal high-fat diet and microplastic exposure on liver health in newborn rat pups. They found that the combination caused more severe liver fat accumulation and oxidative stress damage than either factor alone. The study suggests that prenatal exposure to both microplastics and an unhealthy diet may compound the risk of liver injury in offspring.
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This study reports that sodium butyrate, a postbiotic compound, mitigated microplastic-induced hypertension and kidney dysfunction in juvenile rats by reducing oxidative stress, modulating the gut microbiota, and elevating butyric acid levels.
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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.
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