In vitro assays reveal that histones disrupt mitochondrial function and induce apoptosis in neuronal cells, suggesting potential interventions.
Extracellular histones, emerging as critical inflammatory mediators, have unclear yet significant implications in nerve injury. This study, through in vitro assays using PC-12 and SH-SY5Y neuronal cells, reveals the toxicological mechanisms of histones. Histones trigger calcium influx and disrupt mitochondrial function by opening the MPTP, resulting in a marked decline in MMP. This mitochondrial perturbation further leads to Cyt-C release and upregulation of Caspase-3, triggering apoptotic cell death. However, interventions with MgSO4 and CsA mitigate histone-induced toxicity by blocking calcium influx and inhibiting MPTP opening. These results enhance our understanding of histone-related neurotoxicity and may contribute to developing antidotes against histone-mediated nerve damage at the biochemical and molecular toxicology levels.
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Cao et al. (2025) studied this question.
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