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Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of <t>SOD1</t> (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.
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Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of <t>SOD1</t> (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.
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Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of <t>SOD1</t> (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.
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Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of SOD1 (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.

Journal: International Dental Journal

Article Title: Obesity as a Determinant of Periodontal Therapy Outcomes: Insights on Oxidative and Endoplasmic Reticulum Stress Pathways

doi: 10.1016/j.identj.2026.109472

Figure Lengend Snippet: Oxidative stress markers in the study population, stratified by obesity presence, before and after non-surgical periodontal treatment. Total ROS (A and G), cytosolic superoxide (B and H) and mitochondrial superoxide (C and I) in leukocytes, and protein levels of SOD1 (D and J) in PBMCs normalized to the loading control actin with corresponding WB images (E), and serum total antioxidant capacity (F and K). Data are presented as box and whisker plots and were compared using two-factor analysis of variance (ANOVA) followed by post hoc tests. ** P < .01 when comparing baseline vs 12 wk. # P < .05 when comparing groups with vs without obesity. DCFH, diclorodihidrofluoresceína; dHE, dihydroethidium; MitoSOX, Mitochondrial Superoxide Indicator; ns, not significant; PBMCs, peripheral blood mononuclear cells; ROS, reactive oxygen species; SOD1, superoxide dismutase 1.

Article Snippet: Twenty-five micrograms of protein were separated by SDS-PAGE, transferred to nitrocellulose membranes, blocked, and incubated with the following specific antibodies: rabbit monoclonal anti-superoxide dismutase 1 (SOD1) (Cat# PA5-27240, RRID:AB_2544716), rabbit polyclonal anti-IRE1α (Cat# PA1-46027, RRID:AB_2262265), mouse monoclonal anti-CHOP (Cat# MA1-250, RRID:AB_2292611) from Thermo Fisher Scientific; rabbit polyclonal anti-GRP78 (Cat# ab21685, RRID:AB_2119834), mouse monoclonal anti-ATF6 (Cat# ab122897, RRID:AB_10899) from Abcam; rabbit polyclonal anti-eukaryotic initiation factor 2 phospho (p-eIF2α) (Innovative Research Cat# 44-728G, RRID:AB_15000); mouse monoclonal anti-actin (Cell Signaling Technology Cat# 3700, RRID:AB_2242334) or rabbit polyclonal anti-actin (Sigma-Aldrich Cat# A5060, RRID:AB_476738).

Techniques: Control, Whisker Assay