Fig 1: PREPko cells does not respond to oxidative stress. (A,B) Catalase activity in the HEK-293 and PREPko cells did not show alterations. (C) Superoxide dismutase 1 (SOD1) was statistically increased in the HEK-293 oxidative stress groups compared to the non-stressed HEK-293 group. (D) No differences in SOD1 levels were detected between PREPko groups. (E) Representative images of WB bands for catalase, SOD1 and thioredoxin (Trx) in HEK-293 and PREPko cells in the presence and absence of oxidative stress. Bars represent mean ± SEM. ****p < 0.0005. Univariate analyses of variance with Bonferroni’s adjustment.
Fig 2: Deregulation of redox-homeostasis after Temozolomide treatment in U251 and T98 cells. (A) Spectrophotometric analysis of mitochondrial respiratory chain complex activities measured before and after 24 h of treatment with Temozolomide (TMZ) in U251 and (B) T98 cells. Values are expressed as mean values of complex I, II, I+III and IV normalized for citrate synthase activities (pmol/min/mg of proteins). (C) Descriptive image of Western Blot analysis of representative subunits of the mitochondrial respiratory chain assessed before and after 24 h of treatment with TMZ and their quantification in (D) U251 and (E) T98 cells. Values are expressed as mean values of protein content (arbitrary units) normalized for the signal of PORIN (VDAC). (F) Gene expression profile for detox enzymes (SOD-2, CATALASE, GLUTATHIONE PEROXIDASE -GPX-, GLUTATHIONE SYNTHETASE -GPS-, and REDUCTASE -GR-) after treatment with 100 µM TMZ in U251 and T98 cells. Data were normalized for ß-ACTIN, and the ??Ct values were expressed as FOI of the ratio between treated and control cells. * p < 0.05; ** p < 0.01 vs. control cells. (G) Glutathione concentration assessed after TMZ treatment in both cells by means of a commercially available kit. Data were expressed as glutathione concentration (µM). * p < 0.05 treated vs. control cells. (H) Western blot analysis of CATALASE and SOD in protein lysates from untreated (-) and TMZ-treated (+) U251 and T98 cell lines at 24 h of treatment, and (i) their quantification. Protein signals were normalized to ACTIN levels. * p < 0.05; ** p < 0.01 treated vs. control. Mean values ± SD of three independent experiments.
Fig 3: Western blotting for catalase and SOD-1 in UVA-exposed NhDFs. (A) Representative blot and Ponceau staining. (B) Histograms of densitometric analysis (one-way ANOVA for catalase and SOD-1: p ≤ 0.05; * p ≤ 0.05).
Fig 4: Relative levels of antioxidant enzymes in the control and pathological placenta slices. In the graphs, bars indicate the CATALASE (60 kDa)/ß-actin (42 kDa) ratio and SOD-1 (16 kDa)/ß-actin (42 kDa) ratio densitometric analysis ± SD of twelve independent replicates (n = 12). Asterisks indicate significant differences (* = p < 0.05; ** = p < 0.01) when comparing the pathologies to the control group. CTRL: control group (blue), GDM: gestational diabetes mellitus (purple), SGA: small-for-gestational-age (green).
Fig 5: Effects of resveratrol on oxidative stress status in the ovariectomized model.A–C total antioxidant capacity (T-AOC) (A), catalase (CAT) (B), and superoxide dismutase (SOD) (C) activity in proximal tibias. (D) The protein expression levels of SOD1 and SOD2 were detected by western blot. Data were the means ± SD (n = 6 for each group). ##P < 0.01 vs. Sham group; **P < 0.01 vs. OVX group.
Supplier Page from Abcam for Oxidative Stress Defense (Catalase, SOD1, TRX, smooth muscle Actin) Western Blot Cocktail