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Polystyrene microplastics trigger hepatocyte apoptosis and abnormal glycolytic flux via ROS-driven calcium overload
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This study investigated how polystyrene microplastics damage liver cells and found they trigger a chain reaction involving excess reactive oxygen species (ROS) that leads to calcium overload inside cells. The calcium buildup disrupts normal energy metabolism and ultimately causes liver cell death. The findings reveal a specific molecular pathway connecting microplastic-driven oxidative stress to liver toxicity.
Human health could be affected by the spread of microplastics in the food chain. Our previous research has indicated that microplastics accumulated in the liver and subsequently induce oxidative damage. However, the molecular events linking oxidative stress to calcium ion (Ca) signaling during microplastics stress remains elusive. The present research demonstrated that up-regulation of Orai 1 and stromal interaction molecule 1 (Stim1) expression participated in the microplastics-triggered Ca overload, accompanied with the down-regulation of arcoplasmic reticulum Ca ATPase (SERCA). However, when the protein expression of Stim1/SERCA is restored, microplastics-induced Ca overload is ameliorated. Further analysis revealed that inhibiting the microplastics-induced Ca overload was integral to prevent hepatocyte apoptosis and S phase arrest in the L02 hepatocyte. Simultaneously, we observed that inhibiting microplastics-evoked reactive oxygen species (ROS) could alleviate Ca overload via reversing expression of store-operated Ca channels (SOCs). These changes were accompanied by restoration of glycolytic flux, likely due to the regulation of AMP-activated protein kinase (AMPK)-PGC-1α signaling. Our findings highlight the role of SOCs at microplastics-evoked ROS in Ca overload, and its a crucial step in triggering hepatocyte death. Collectively, this study reveals a regulatory paradigm that links ROS with AMPK and Ca signaling in microplastics-triggered hepatotoxicity.
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ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
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This study found that polystyrene nanoplastics damage human liver cells by triggering harmful interactions between reactive oxygen species (ROS) and a protein called DRP1 that controls mitochondria. The nanoplastics caused mitochondria to break apart, leading to cell injury and death. This research helps explain how microplastic exposure could contribute to liver damage in humans at the cellular level.
Activation of pyroptosis and ferroptosis is involved in the hepatotoxicity induced by polystyrene microplastics in mice
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Researchers exposed mice to polystyrene microplastics and found that the particles caused significant liver damage, including structural changes and impaired function. The study identified two specific cell death pathways, pyroptosis and ferroptosis, as key mechanisms driving the liver injury. These findings suggest that microplastic exposure may harm liver health through multiple biological pathways that warrant further investigation.
Polystyrene microplastics induce hepatic lipid metabolism and energy disorder by upregulating the NR4A1-AMPK signaling pathway
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Researchers found that polystyrene microplastics accumulate in the liver and disrupt fat and energy metabolism by activating a specific molecular pathway called NR4A1-AMPK. This activation triggers a self-cleaning process called autophagy that reduces fat production in liver cells, while also increasing harmful reactive oxygen species. The findings suggest that long-term microplastic exposure could lead to ongoing liver damage through this metabolic disruption.
Polystyrene microplastics induce hepatotoxicity and disrupt lipid metabolism in the liver organoids
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Using lab-grown human liver organoids, researchers showed that polystyrene microplastics caused liver cell damage even at concentrations found in the environment. The microplastics disrupted fat metabolism, increased harmful reactive oxygen species, and triggered inflammation in the liver tissue. This study provides early evidence that microplastic exposure could contribute to liver problems like fatty liver disease in humans.
Polystyrene microplastics exposure aggravates acute liver injury by promoting Kupffer cell pyroptosis
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Researchers found that long-term exposure to polystyrene microplastics worsened acute liver injury in mice by triggering a specific type of inflammatory cell death called pyroptosis in liver immune cells. When they blocked this cell death pathway either genetically or with a drug, the damaging effects of the microplastics were significantly reduced. The study suggests that microplastic exposure may make the liver more vulnerable to injury by amplifying inflammatory responses.
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