El-Alfy Nagla Zaky Ibrahim, Emam Asmaa Ahmed Khaled, Mahmoud Mahmoud Fathy, Morgan Omnia Nabeel Mohamed, El-Ashry Sally Ramadan Gabr Eid
Biological and Geological Sciences Department, Faculty of Education, Ain Shams University, El-Khalyfa El-Mamoun Street Abbasya, Cairo 11341, Egypt.
Toxicol Rep. 2024 Nov 22;13:101828. doi: 10.1016/j.toxrep.2024.101828. eCollection 2024 Dec.
Vitamin D (Vit D) has gained significant attention in health research recently as a result of its potential protective effects against various cellular damages. This study aimed to investigate the ability of vitamin D to mitigate deoxyribonucleic acid (DNA) fragmentation in liver cells and bone marrow cytotoxicity induced by chloramphenicol (CAP). Sixty male albino mice were divided into six groups: control, chloramphenicol-treated (250 and 500 mg/kg body weight, 5 days per week for 4 weeks), vitamin D-treated (800 IU/kg body weight, 5 days per week for 4 weeks) and vitamin D plus chloramphenicol-treated groups. Results of DNA fragmentation test revealed that oral treatment with low and high doses of CAP significantly increased the frequency of DNA fragmentation in liver cells in comparison with the control, whereas oral treatment with vitamin D alone or plus low and high doses of chloramphenicol significantly reduced the genotoxicity in liver cells in comparison with the control group. Micronucleus analysis showed that CAP treatment at low and high doses significantly increased micronuclei formation and cytotoxicity in bone marrow cells. However, vitamin D significantly reduced the micronuclei formation in bone marrow cells of mice treated with chloramphenicol. Vitamin D alone showed no significant difference in the frequency of micronuclei and bone marrow cytotoxicity compared to the control group. Accordingly, further research exploring the mechanisms underlying the protective effects of vitamin D and investigating optimal dosing regimens is warranted. Also, clinical studies evaluating the efficacy of vitamin D supplementation to mitigate the adverse effects of chloramphenicol in human patients are recommended.
维生素D（Vit D）由于其对各种细胞损伤的潜在保护作用，最近在健康研究中受到了广泛关注。本研究旨在探讨维生素D减轻氯霉素（CAP）诱导的肝细胞脱氧核糖核酸（DNA）片段化和骨髓细胞毒性的能力。将60只雄性白化小鼠分为六组：对照组、氯霉素处理组（250和500mg/kg体重，每周5天，共4周）、维生素D处理组（800IU/kg体重，每周5天，共4周）以及维生素D加氯霉素处理组。DNA片段化测试结果显示，与对照组相比，低剂量和高剂量的CAP口服处理显著增加了肝细胞中DNA片段化的频率，而单独口服维生素D或与低剂量和高剂量氯霉素联合使用时，与对照组相比，显著降低了肝细胞中的遗传毒性。微核分析表明，低剂量和高剂量的CAP处理显著增加了骨髓细胞中的微核形成和细胞毒性。然而，维生素D显著降低了氯霉素处理小鼠骨髓细胞中的微核形成。单独使用维生素D与对照组相比，微核频率和骨髓细胞毒性无显著差异。因此，有必要进一步研究探索维生素D保护作用的潜在机制并研究最佳给药方案。此外，建议开展临床研究，评估补充维生素D以减轻氯霉素对人类患者不良影响的疗效。
