Long-Term Exposure to Tire-Derived 6-PPD Quinone Causes Neurotoxicity and Neuroinflammation via Inhibition of HTR2A in C57BL/6 Mice.

-(1,3-dimethylbutyl)-'-phenyl--phenylenediamine quinone (6-PPDQ), a novel contaminant derived from tire wear, has raised concerns due to its potential neurotoxicity, yet its long-term effects on mammalian neurological health remain poorly understood. This study investigates the neurotoxic and neuroinflammatory impacts of prolonged 6-PPDQ exposure using male C57BL/6 mice. Behavioral assessments revealed significant cognitive deficits, while biochemical analyses demonstrated increased levels of reactive oxygen species, apoptosis, and blood-brain barrier (BBB) disruption.

Neurotoxicity from long-term exposure to 6-PPDQ: Recent advances.

The recent acceleration of industrialization and urbanization has brought significant attention to N-(1,3-Dimethylbutyl)-N'-phenyl-p-phenylenediamine quinone (6-PPDQ), an emerging environmental pollutant from tire wear, due to its long-term effects on the environment and organisms. Recent studies suggest that 6-PPDQ can disrupt neurotransmitter synthesis and release, impact receptor function, and alter signaling pathways, potentially causing oxidative stress, inflammation, and apoptosis. This review investigates the potential neurotoxic effects of prolonged 6-PPDQ exposure, the mechanisms underlying its cytotoxicity, and the associated health risks.

Early versus Delayed Hepatectomy for Spontaneously Ruptured Hepatocellular Carcinoma: A Systematic Review and Meta-Analysis.

Objective: Here, we aimed to compare early hepatectomy (EH) with delayed hepatectomy (DH) as a treatment for spontaneously ruptured hepatocellular carcinoma (HCC).

Methods: Several databases were systematically searched for eligible studies that compared DH with EH for spontaneously ruptured HCC treatment. Studies that met the inclusion criteria were reviewed systematically, and the reported data were aggregated statistically, using the RevMan v5.