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<p>Buprofezin (BPFN), an extensively used insecticide, has raised concerns due to its potential genotoxic and pro-inflammatory effects in non-target organisms. This study aimed to assess the extent of BPFN-induced genotoxicity and inflammation in Balb/c mice and to evaluate the protective roles of two natural antioxidants, Vitamin C and curcumin (CUR). Male mice were orally administered BPFN at doses of 50, 100, and 250 mg/kg body weight for 28 days. Vitamin C and CUR (100 mg/kg each) were given individually or in combination. Genotoxicity was evaluated using the comet assay, which revealed significant DNA damage in both liver and kidney tissues, reflected by marked increases in comet length, head length, tail length, and olive tail moment (<i>p</i> &lt; 0.001). Co-treatment with Vit C and CUR significantly reduced these genotoxic parameters (<i>p</i> &lt; 0.001). Quantitative PCR analysis showed that BPFN exposure upregulated Interleukin-1β (IL-1β) mRNA expression by 4.28- to 7.94-fold in liver and 2.68- to 5.36-fold in kidney tissues (<i>p</i> &lt; 0.001), while Interleukin-6 (IL-6) and TNF-α levels were also elevated and subsequently downregulated after antioxidant administration. Molecular docking analysis revealed that CUR had higher binding affinities with NF-κB (-9.8 kJ/mol) and TNF-α (-8.8 kJ/mol), whereas Vitamin C exhibited lower affinities (-6.2 kJ/mol for NF-κB and − 6.7 kJ/mol for TNF-α). Molecular dynamics simulations demonstrated that CUR maintained more stable interactions, with RMSD values ranging from 0.8 to 1.5 Å, compared to Vitamin C (0.5 to 2.0 Å). These findings highlight the protective efficacy of Vitamin C and curcumin—particularly in combination—against BPFN-induced genotoxic and inflammatory damage, suggesting their potential as mitigating agents in environmental toxicology contexts.</p>

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Molecular Simulation and Expression Analysis of Vitamin C and Curcumin in Mitigating Buprofezin-induced Genotoxicity and Inflammatory Responses in Balb/c Mice

  • 期刊论文

  • 发表日期：

    2025年9月18日

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  • Haleema Sadia,
  • Irfan Zia Qureshi,
  • Muhammad Naveed,
  • Tariq Aziz,
  • Manal F. Elkhadragy,
  • Maher S. Alwethaynani,
  • Fahad Al-Asmari,
  • Areej A Alhhazmi,
  • Hanan Abdulrahman Sagini,
  • Suad Hamdan Almasoudi,
  • Fakhria A. Al-Joufi

摘要

Buprofezin (BPFN), an extensively used insecticide, has raised concerns due to its potential genotoxic and pro-inflammatory effects in non-target organisms. This study aimed to assess the extent of BPFN-induced genotoxicity and inflammation in Balb/c mice and to evaluate the protective roles of two natural antioxidants, Vitamin C and curcumin (CUR). Male mice were orally administered BPFN at doses of 50, 100, and 250 mg/kg body weight for 28 days. Vitamin C and CUR (100 mg/kg each) were given individually or in combination. Genotoxicity was evaluated using the comet assay, which revealed significant DNA damage in both liver and kidney tissues, reflected by marked increases in comet length, head length, tail length, and olive tail moment (p < 0.001). Co-treatment with Vit C and CUR significantly reduced these genotoxic parameters (p < 0.001). Quantitative PCR analysis showed that BPFN exposure upregulated Interleukin-1β (IL-1β) mRNA expression by 4.28- to 7.94-fold in liver and 2.68- to 5.36-fold in kidney tissues (p < 0.001), while Interleukin-6 (IL-6) and TNF-α levels were also elevated and subsequently downregulated after antioxidant administration. Molecular docking analysis revealed that CUR had higher binding affinities with NF-κB (-9.8 kJ/mol) and TNF-α (-8.8 kJ/mol), whereas Vitamin C exhibited lower affinities (-6.2 kJ/mol for NF-κB and − 6.7 kJ/mol for TNF-α). Molecular dynamics simulations demonstrated that CUR maintained more stable interactions, with RMSD values ranging from 0.8 to 1.5 Å, compared to Vitamin C (0.5 to 2.0 Å). These findings highlight the protective efficacy of Vitamin C and curcumin—particularly in combination—against BPFN-induced genotoxic and inflammatory damage, suggesting their potential as mitigating agents in environmental toxicology contexts.