Fig. 2

Parkin lowers chronic oxidative stress-induced damage in the cytosol of mammalian brain. a, b Total protein nitrotyrosination in midbrain homogenates from 6 month-old mice of indicated genotypes, where each lane represents a separate mouse. Ponceau S was used as a loading control to quantify relative nitrotryrosine signals (b). c Total protein nitrotyrosination in cytoplasmic (C) versus mitochondrial (M) fractions from midbrains of 6 month-old mice. d Relative, mean protein carbonyl content in brain homogenates from 6 month-old mice, and e homogenates of human frontal cortices from control subjects and age- and ethnicity-matched, parkin-deficient autosomal recessive Parkinson disease (ARPD) patients as well as from age-matched, non-PRKN-linked parkinsonism (PSM) cases. f Relative, mean protein carbonyl content of brain mitochondria and in g of cytosolic fractions from 6-month-old WT, prkn^± and prkn^−/− mice. Data in b–g represent n = 3–4/genotype ± SEM. Significance was determined using a 1-way ANOVA with Tukey’s post-hoc analysis (b, d–g), where *p ≤ 0.05, **p ≤ 0.01, and ***p ≤ 0.001