FIG. 3.

Peroxisome turnover in (A–C) normal cells and in (D–F) cells with impaired pexophagy after stimulation with endotoxin (ET). (A–C) In normal cells, endotoxin causes slight impairment of the peroxisomal redox state. The simultaneous activation of pexophagy eliminates compromised organelles and helps to preserve the cellular redox balance. The second phase is characterized by proliferation of peroxisomes, which leads to quantitative and qualitative restoration of a functional peroxisomal pool. (D–F) Impaired pexophagy results in accumulation of dysfunctional peroxisomes with increased intraorganellar oxidative stress. Endotoxin further exacerbates peroxisomal redox imbalance and worsens intraorganellar homeostasis. Compromised maintenance mechanisms due to impaired pexophagy perpetuate oxidative stress and result in gradual deterioration of peroxisomal (peroxisome burnout) and later cellular homeostasis. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars