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<p>5-Fluorouracil (5-FU) constitutes one of the most potent antineoplastic medicines, utilized for managing a variety of malignancies and associated with considerable hepatic damage. Chia oil, or Salba, possesses diverse pharmacological characteristics, which could be ascribed to a rise in omega-3 nutritional concentrations. This investigation attempted to examine the preventive actions and mechanistic pathways behind chia oil supplementation in a 5-FU-aggravated hepatic injury murine model. Twenty-four male mice (<i>n</i> = 6) were randomly assigned into four groups, namely, control, 5-FU, and chia oil + 5-FU treatment groups. Chia oil was orally administered at small (1900&#xa0;mg per kg) and large (3800&#xa0;mg per kg) dosages for 7&#xa0;days, whereas 5-FU was injected intraperitoneally (400&#xa0;mg/kg; three doses at days 4–6). Biochemical, histopathological, and molecular variables were determined. Gas chromatography (GC-FID) analysis verified the existence of bioactive fatty components in chia oil. 5-FU application produced profound elevation in serum ALT, AST, MDA, and pro-inflammatory cytokines, accompanied by impaired antioxidant defense and downregulation of Nrf2/SLC7A11/GPX4 expression. Co-treatment with chia oil markedly attenuated these alterations by restoring the activities of antioxidant enzymes, lowering lipid peroxidation, and improving liver histology. Gas chromatography (GC-FID) analysis confirmed that α-linolenic acid (62.5%) was represented as the identified fatty acyl compound, succeeded by different elements comprising linoleic, oleic, palmitic, and stearic acyl derivatives. Low and high doses of chia oil attenuated 5-FU-induced hepatic injury via the Nrf2-SLC7A11 signaling modulation, inhibiting ferroptosis.</p>

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Counteractive effect of chia seed oil extract on 5-fluorouracil-induced hepatotoxicity through targeting the Nrf2/SLC7A11/GPX4 axis

  • 期刊论文

  • 发表日期：

    2026年5月2日

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  • Ali Jihad Hemid Al-Athari,
  • Zinah Essam Hameed,
  • Ahmed Khalid Aldhalmi,
  • Saja Majeed Shareef,
  • Hayder Ridha-Salman,
  • Khulood Majid Alsaraf

摘要

5-Fluorouracil (5-FU) constitutes one of the most potent antineoplastic medicines, utilized for managing a variety of malignancies and associated with considerable hepatic damage. Chia oil, or Salba, possesses diverse pharmacological characteristics, which could be ascribed to a rise in omega-3 nutritional concentrations. This investigation attempted to examine the preventive actions and mechanistic pathways behind chia oil supplementation in a 5-FU-aggravated hepatic injury murine model. Twenty-four male mice (n = 6) were randomly assigned into four groups, namely, control, 5-FU, and chia oil + 5-FU treatment groups. Chia oil was orally administered at small (1900 mg per kg) and large (3800 mg per kg) dosages for 7 days, whereas 5-FU was injected intraperitoneally (400 mg/kg; three doses at days 4–6). Biochemical, histopathological, and molecular variables were determined. Gas chromatography (GC-FID) analysis verified the existence of bioactive fatty components in chia oil. 5-FU application produced profound elevation in serum ALT, AST, MDA, and pro-inflammatory cytokines, accompanied by impaired antioxidant defense and downregulation of Nrf2/SLC7A11/GPX4 expression. Co-treatment with chia oil markedly attenuated these alterations by restoring the activities of antioxidant enzymes, lowering lipid peroxidation, and improving liver histology. Gas chromatography (GC-FID) analysis confirmed that α-linolenic acid (62.5%) was represented as the identified fatty acyl compound, succeeded by different elements comprising linoleic, oleic, palmitic, and stearic acyl derivatives. Low and high doses of chia oil attenuated 5-FU-induced hepatic injury via the Nrf2-SLC7A11 signaling modulation, inhibiting ferroptosis.