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Background <p>Cyclophosphamide (CP) is a widely used chemotherapeutic agent against various cancers. However, its clinical utility is often limited by significant side effects, including nephrotoxicity. This study elucidated the possible benefits of the antioxidant and mucolytic agent, carbocisteine (S-carboxymethylcysteine (SCMC)), against CP-induced renal damage.</p> Methods <p>Rats received 250&#xa0;mg/kg orally of SCMC for 7&#xa0;days and a single injection of 100&#xa0;mg/kg of CP on day 5.</p> Results <p>CP caused kidney injury manifested by elevated serum kidney function markers (creatinine, BUN, and uric acid), histopathological alterations, oxidative stress, and inflammation. SCMC restored markers of renal function and maintained the histological integrity of the kidneys. SCMC effectively attenuated oxidative stress by reducing malondialdehyde and increasing GSH content and SOD and catalase activities. Additionally, SCMC suppressed CP-induced upregulation of NF-κB, reduced pro-inflammatory cytokines, and downregulated caspase-3 levels in the kidney of rats. These effects were linked to downregulation of Keap-1, upregulation of Nrf2, and increased HO-1 both activity and expression.</p> Conclusion <p>SCMC attenuates CP nephrotoxicity by mitigating oxidative damage, inflammatory response, and apoptosis, and enhancement of the Nrf2/HO-1 signaling. These findings highlight the potential of SCMC as a protective agent against chemotherapy-induced kidney damage.</p>

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Protective role of S-carboxymethylcysteine against cyclophosphamide nephrotoxicity: involvement of Nrf2/HO-1 signaling and suppression of oxidative stress, inflammation, and apoptosis

  • 期刊论文

  • 发表日期：

    2025年10月29日

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  • Reem S. Alruhaimi,
  • Emad H. M. Hassanein,
  • Sulaiman M. Alnasser,
  • Ahmad F. Ahmeda,
  • Hanan S. Althagafy,
  • Mostafa Sabry,
  • Abdullatif A. Ahmed,
  • Ayman M. Mahmoud

摘要

Background

Cyclophosphamide (CP) is a widely used chemotherapeutic agent against various cancers. However, its clinical utility is often limited by significant side effects, including nephrotoxicity. This study elucidated the possible benefits of the antioxidant and mucolytic agent, carbocisteine (S-carboxymethylcysteine (SCMC)), against CP-induced renal damage.

Methods

Rats received 250 mg/kg orally of SCMC for 7 days and a single injection of 100 mg/kg of CP on day 5.

Results

CP caused kidney injury manifested by elevated serum kidney function markers (creatinine, BUN, and uric acid), histopathological alterations, oxidative stress, and inflammation. SCMC restored markers of renal function and maintained the histological integrity of the kidneys. SCMC effectively attenuated oxidative stress by reducing malondialdehyde and increasing GSH content and SOD and catalase activities. Additionally, SCMC suppressed CP-induced upregulation of NF-κB, reduced pro-inflammatory cytokines, and downregulated caspase-3 levels in the kidney of rats. These effects were linked to downregulation of Keap-1, upregulation of Nrf2, and increased HO-1 both activity and expression.

Conclusion

SCMC attenuates CP nephrotoxicity by mitigating oxidative damage, inflammatory response, and apoptosis, and enhancement of the Nrf2/HO-1 signaling. These findings highlight the potential of SCMC as a protective agent against chemotherapy-induced kidney damage.