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<p>Hexavalent chromium [Cr(VI)] is a highly toxic environmental pollutant that induces severe renal injury primarily through oxidative stress, inflammation, DNA damage, and dysregulation of cell death pathways. Thymoquinone (Tq) has been reported to exert antioxidant and anti-inflammatory effects; however, its potential protective role against Cr(VI)-induced nephrotoxicity remains unclear. This study aimed to investigate the protective effects of Tq against Cr(VI)-induced renal injury, focusing on oxidative stress, inflammation, DNA damage, apoptosis, and ferroptosis-related markers. Forty male Wistar albino rats were randomly assigned into five groups (n = 8): Control, vehicle, Cr(VI) (15&#xa0;mg/kg), Tq (30&#xa0;mg/kg), and Cr(VI) + Tq. All treatments were administered orally for 10&#xa0;days. Biochemical analyses included malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), transforming growth factor-beta 1 (TGF-β1), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels. Histopathological, histometric, and immunohistochemical evaluations (GPX4, ACSL4, Caspase-3) were also performed. Cr(VI) exposure significantly increased MDA, TNF-α, NF-κB, TGF-β1, and 8-OHdG levels, while decreasing GSH, SOD, and CAT activities (p &lt; 0.01). These changes were associated with marked histopathological damage, renal dysfunction reflected by elevated serum BUN and creatinine levels, decreased GPX4 expression, and increased ACSL4 and Caspase-3 levels in renal tissue, suggesting the involvement of ferroptotic and apoptotic pathways. Tq treatment significantly ameliorated these alterations by restoring antioxidant defenses, suppressing inflammation and fibrosis, reducing DNA damage, and modulating markers of ferroptosis and apoptosis (p &lt; 0.01). In conclusion, Tq attenuates Cr(VI)-induced nephrotoxicity, as evidenced by improvements in oxidative stress, inflammation, DNA damage, ferroptosis- and apoptosis-related markers, together with preservation of renal structure and function.</p> Graphical abstract <p></p>

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Protective effects of thymoquinone against hexavalent chromium-ınduced nephrotoxicity: a multiparametric evaluation of oxidative stress, ınflammation, ferroptosis- and apoptosis-related markers

  • 期刊论文

  • 发表日期：

    2026年7月22日

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  • Tansu Kusat,
  • Feyza Basak,
  • Eyup Altınoz,
  • Yasemin Bıcer,
  • Mert Uge

摘要

Hexavalent chromium [Cr(VI)] is a highly toxic environmental pollutant that induces severe renal injury primarily through oxidative stress, inflammation, DNA damage, and dysregulation of cell death pathways. Thymoquinone (Tq) has been reported to exert antioxidant and anti-inflammatory effects; however, its potential protective role against Cr(VI)-induced nephrotoxicity remains unclear. This study aimed to investigate the protective effects of Tq against Cr(VI)-induced renal injury, focusing on oxidative stress, inflammation, DNA damage, apoptosis, and ferroptosis-related markers. Forty male Wistar albino rats were randomly assigned into five groups (n = 8): Control, vehicle, Cr(VI) (15 mg/kg), Tq (30 mg/kg), and Cr(VI) + Tq. All treatments were administered orally for 10 days. Biochemical analyses included malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), tumor necrosis factor-alpha (TNF-α), nuclear factor kappa B (NF-κB), transforming growth factor-beta 1 (TGF-β1), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels. Histopathological, histometric, and immunohistochemical evaluations (GPX4, ACSL4, Caspase-3) were also performed. Cr(VI) exposure significantly increased MDA, TNF-α, NF-κB, TGF-β1, and 8-OHdG levels, while decreasing GSH, SOD, and CAT activities (p < 0.01). These changes were associated with marked histopathological damage, renal dysfunction reflected by elevated serum BUN and creatinine levels, decreased GPX4 expression, and increased ACSL4 and Caspase-3 levels in renal tissue, suggesting the involvement of ferroptotic and apoptotic pathways. Tq treatment significantly ameliorated these alterations by restoring antioxidant defenses, suppressing inflammation and fibrosis, reducing DNA damage, and modulating markers of ferroptosis and apoptosis (p < 0.01). In conclusion, Tq attenuates Cr(VI)-induced nephrotoxicity, as evidenced by improvements in oxidative stress, inflammation, DNA damage, ferroptosis- and apoptosis-related markers, together with preservation of renal structure and function.

Graphical abstract