Ascorbate prevents spontaneous liver tumor development in mice with double deficiency of superoxide dismutase 1 and peroxiredoxin 4

NASH developed in Sod1- and Prdx4-double KO mice progressed to hepatic tumors.
Supplementation of ascorbate (Asc) effectively suppressed the tumor development.
Upregulated amino acid metabolisms in precancerous cells likely supports tumorigenic growth.
Asc appears to induce ferroptosis in cells destined for tumorigenic transformation.

在超氧化物歧化酶1（Sod1）与过氧化物还原酶4（Prdx4）双基因敲除小鼠中发生的非酒精性脂肪性肝炎（NASH）可进展为肝脏肿瘤。
补充抗坏血酸（Asc）可有效抑制该肿瘤的发生与发展。
癌前细胞内上调的氨基酸代谢或可助力肿瘤性生长。
抗坏血酸似乎可在即将发生肿瘤性转化的细胞中诱导铁死亡（ferroptosis）。