Hafiz Muhammad Aslam, Azka Sohail, Ammara Shahid, Maham Abdul Bari Khan, Muhammad Umar Sharif, Razia Kausar, Samia Nawab, Waqas Farooq, Kashif Jilani, Majeeda Rasheed
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引用次数: 0
Abstract
Background: Levofloxacin, a fluoroquinolone, is an extensively used antibiotic effective against both positively and negatively staining bacteria. It works by inhibiting bacterial topoisomerase type II and topoisomerase type IV, resulting in impaired DNA synthesis and bacterial cell death. Eryptosis is another term for apoptotic cell death of erythrocyte marked by cell shrinkage, phosphatidylserine (PS) flipping, and membrane blebbing.
Methods: The intent of the present research was to look at the eryptotic effect of levofloxacin by exposing erythrocytes to therapeutical doses (7, 14 µM) of levofloxacin for 48 hours. Cell size evaluation, PS subjection to outside, and calcium channel inhibition were carried out to investigate eryptosis. Oxidative stress generated by levofloxacin was measured as a putative mechanism of eryptosis using glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase activities. Similarly, hemolysis measurements demonstrated levofloxacin's cytotoxic effect.
Results: Our findings showed that therapeutic doses of levofloxacin can cause a considerable decline in antioxidant enzymes activities, as well as induce cell shrinkage, PS externalization, and hemolysis in erythrocytes. The role of calcium in triggering erythrocyte shrinkage was also confirmed.
Conclusion: In conclusion, our findings showed that the indicated levofloxacin doses caused oxidative stress, which leads to erythrocyte death via eryptosis and hemolysis. These findings emphasize the importance of using levofloxacin with caution and the need for additional research to mitigate these side effects.
背景:左氧氟沙星是一种氟喹诺酮类药物,是一种广泛使用的抗生素,对阳性和阴性染色细菌均有效。它通过抑制细菌的拓扑异构酶 II 型和拓扑异构酶 IV 型,导致 DNA 合成受损和细菌细胞死亡。红细胞凋亡(Eryptosis)是红细胞凋亡细胞死亡的另一个术语,以细胞萎缩、磷脂酰丝氨酸(PS)翻转和膜破裂为特征:本研究的目的是通过将红细胞置于治疗剂量(7、14 µM)的左氧氟沙星中 48 小时来观察左氧氟沙星的凋亡效应。通过评估细胞大小、PS 受外界影响和钙通道抑制来研究红细胞凋亡。利用谷胱甘肽过氧化物酶(GPx)、超氧化物歧化酶(SOD)和过氧化氢酶的活性测量了左氧氟沙星产生的氧化应激作为红细胞沉降的推定机制。同样,溶血测定也证明了左氧氟沙星的细胞毒性作用:结果:我们的研究结果表明,治疗剂量的左氧氟沙星可导致抗氧化酶活性大幅下降,并诱导细胞萎缩、PS外化和红细胞溶血。钙在引发红细胞萎缩中的作用也得到了证实:总之,我们的研究结果表明,指定剂量的左氧氟沙星会引起氧化应激,导致红细胞因红细胞凋亡和溶血而死亡。这些发现强调了谨慎使用左氧氟沙星的重要性,以及开展更多研究以减轻这些副作用的必要性。