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<p>Purpose: We hypothesized that the curcumin analogs C66 and B2BrBC influenced inflammation in cancer cells by modulating free radical production and oxidative stress. Methods: We tested human breast cancer epithelial MDA-MB-231 and non-cancerous MCF-10&#xa0;A cells. Results: The tested compounds significantly increased lipid peroxidation (TBARS) in both cell lines; curcumin induced a stronger effect in MDA-MB-231, C66 in MCF-10&#xa0;A, and B2BrBC showed pronounced prooxidant activity in both cell lines. The baseline antioxidant activity (AOA) was higher in MCF-10&#xa0;A cells. Curcumin exhibited limited or even suppressive effects, whereas C66 and B2BrBC markedly enhanced AOA in both cell lines, with a stronger effect observed in MCF-10&#xa0;A cells. Curcumin and its analogs strongly enhanced superoxide dismutase (SOD) activity in MDA-MB-231 cancer cells but suppressed SOD activity in non-tumorigenic MCF-10&#xa0;A cells. They exerted opposite effects on catalase (CAT) activity: strong suppression in MCF-10&#xa0;A cells but a marked increase in MDA-MB-231 cells. Glutathione Reductase (GR) activity was substantially enhanced in both cell lines, with MCF-10&#xa0;A showing the strongest response to B2BrBC, and MDA-MB-231 cells showing the strongest response to C66. Conclusions: Curcumin, C66, and B2BrBC modulated oxidative stress in a cell type-specific manner. MDA-MB-231 cells showed upregulation of the antioxidant enzyme activity. This highlights the potential of these analogs to regulate the redox balance in cancer cells.</p>

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The Effect of Curcumin and its Analogs C66 and B2BrBC on Key Biomarkers of Oxidative Stress in Breast Cancer Cells

  • 期刊论文

  • 发表日期：

    2026年4月17日

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  • Elitsa Pavlova,
  • Radoslav Stojchevski,
  • Nikola Hadzi-Petrushev,
  • Jane Bogdanov,
  • Mitko Mladenov,
  • Dimiter Avtanski

摘要

Purpose: We hypothesized that the curcumin analogs C66 and B2BrBC influenced inflammation in cancer cells by modulating free radical production and oxidative stress. Methods: We tested human breast cancer epithelial MDA-MB-231 and non-cancerous MCF-10 A cells. Results: The tested compounds significantly increased lipid peroxidation (TBARS) in both cell lines; curcumin induced a stronger effect in MDA-MB-231, C66 in MCF-10 A, and B2BrBC showed pronounced prooxidant activity in both cell lines. The baseline antioxidant activity (AOA) was higher in MCF-10 A cells. Curcumin exhibited limited or even suppressive effects, whereas C66 and B2BrBC markedly enhanced AOA in both cell lines, with a stronger effect observed in MCF-10 A cells. Curcumin and its analogs strongly enhanced superoxide dismutase (SOD) activity in MDA-MB-231 cancer cells but suppressed SOD activity in non-tumorigenic MCF-10 A cells. They exerted opposite effects on catalase (CAT) activity: strong suppression in MCF-10 A cells but a marked increase in MDA-MB-231 cells. Glutathione Reductase (GR) activity was substantially enhanced in both cell lines, with MCF-10 A showing the strongest response to B2BrBC, and MDA-MB-231 cells showing the strongest response to C66. Conclusions: Curcumin, C66, and B2BrBC modulated oxidative stress in a cell type-specific manner. MDA-MB-231 cells showed upregulation of the antioxidant enzyme activity. This highlights the potential of these analogs to regulate the redox balance in cancer cells.