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Nickel(II)-induced nasal epithelial toxicity and oxidative mitochondrial damage
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文摘

Nickel(II) has growth-inhibiting and apoptosis-activating effects on RPMI-2650 cells.

p53 is involved in arresting damaged cells at G2/M checkpoint and inducing apoptosis.

ROS-mediated mitochondrial damage is a possible mechanism of nickel(II) toxicity.

NAC can help protect against the harmful effects of nickel(II) on the nasal mucosa.

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