Gentamycin sulfate is an aminoglycoside antibiotic that inhibits the growth of Gram-positive and Gram-negative bacteria and several strains of mycoplasma in tissue culture[1]. Gentamicin sulfate inhibits the activity of deoxyribonuclease I with an IC50 value of 0.57±0.12mM[2]. Gentamycin sulfate acts as a protein synthesis inhibitor, binding irreversibly to the small 16S rRNA of the 30S ribosomal subunit and interfering with protein synthesis, a mechanism of action similar to that of other aminoglycosides[3]. Gentamycin sulfate is used to treat a variety of bacterial infections. It is poorly absorbed orally and can be administered intramuscularly or intravenously[4]. Gentamycin sulfate is a potent antibiotic that is widely used in human and animal cell culture. The recommended concentration is usually 50μg/ml, but caution is required when using it in plant cell lines. The recommended concentration is 10μg/ml or lower [5, 6].
In vitro, treatment of human neutrophils with gentamycin sulfate (0-200μM) for 1h significantly inhibited NADPH oxidase activity and concentration-dependently inhibited superoxide production in neutrophils exposed to phorbol myristate [5]. Gentamycin Sulfate (25, 100, 400 μg/mL) treated human osteoblasts (hFOB 1.19) for 6 hours, dose-dependently reduced alkaline phosphatase (ALP) activity, inhibited cell proliferation, survival and adhesion ability [6].
In vivo, gentamycin sulfate (50, 100 mg/kg/day) was intravenously injected into male Sprague Dawley rats for 7 days, which led to increased expression of kidney injury molecule 1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL) in a dose- and time-dependent manner, inducing a rat nephrotoxicity model [7].
References:
[1] Rudin A, Healey A, Phillips C A, et al. Antibacterial activity of gentamicin sulfate in tissue culture[J]. Applied microbiology, 1970, 20(6): 989-990.
[2] Xu W, Xie Z, Tong C, et al. A rapid and sensitive method for kinetic study and activity assay of DNase I in vitro based on a GO-quenched hairpin probe[J]. Analytical and Bioanalytical Chemistry, 2016, 408: 3801-3809.
[3] Kumar C, Himabindu M, Jetty A. Microbial biosynthesis and applications of gentamicin: a critical appraisal[J]. Critical reviews in biotechnology, 2008, 28(3): 173-212.
[4] Nwakile D C, Dozie-Nwakile O C, Okoye E I, et al. Non-Absorbable Oral Gentamicin Sulphate: Biopharmaceutical and Dosage Form Evaluation[J]. European Pharmaceutical Journal, 2021, 68(2): 8-15.
[5] Schafer T W, Pascale A, Shimonaski G, et al. Evaluation of gentamicin for use in virology and tissue culture[J]. Applied Microbiology, 1972, 23(3): 565-570.
[6] Dodds J H, Roberts L W. Some inhibitory effects of gentamicin on plant tissue cultures[J]. In Vitro, 1981, 17: 467-470.
[7] Umeki S. Anti-inflammatory action of gentamycin through inhibitory effect on neutrophil NADPH oxidase activity[J]. Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, 1995, 110(4): 817-821.
[8] Ince A, Schütze N, Hendrich C, et al. In vitro investigation of orthopedic titanium-coated and brushite-coated surfaces using human osteoblasts in the presence of gentamycin[J]. The Journal of arthroplasty, 2008, 23(5): 762-771.
[9] Luo Q H, Chen M L, Chen Z L, et al. Evaluation of KIM-1 and NGAL as early indicators for assessment of gentamycin-induced nephrotoxicity in vivo and in vitro[J]. Kidney and Blood Pressure Research, 2016, 41(6): 911-918.
硫酸庆大霉素（Gentamycin Sulfate）是一种氨基糖苷类抗生素，可抑制革兰氏阳性和革兰氏阴性细菌的生长，并抑制组织培养中的几种支原体菌株[1]。Gentamicin sulfate可抑制脱氧核糖核酸酶（DNase I）的活性，IC50值为0.57±0.12mM[2]。Gentamycin Sulfate起到蛋白质合成抑制剂的作用，不可逆地与30S核糖体亚基的小16S rRNA结合，干扰蛋白质合成，这种作用机制类似于其他氨基糖苷类药物[3]。Gentamycin Sulfate用于治疗多种类型的细菌感染，口服吸收差，可以通过肌肉或静脉注射给药[4]。Gentamycin Sulfate是一种有效的抗生素，广泛应用于人类和动物细胞培养中，通常推荐的浓度为50μg/ml，但在植物细胞系中使用时需要谨慎，推荐浓度为10μg/ml或更低[5, 6]。
在体外，Gentamycin Sulfate（0-200μM）处理人类中性粒细胞1h，显著抑制了NADPH氧化酶活性，浓度依赖性地抑制了暴露于佛波醇肉豆蔻酸酯的中性粒细胞的超氧化物生成[7]。Gentamycin Sulfate（25、100、400μg/mL）处理人成骨细胞（hFOB 1.19）6h，剂量依赖性地降低了碱性磷酸酶（ALP）活性，抑制了细胞的增殖、存活和粘附能力[8]。
在体内，Gentamycin Sulfate（50，100mg/kg/day）通过静脉注射处理雄性Sprague Dawley大鼠7天，剂量和时间依赖性地导致了肾损伤分子1（KIM-1）和中性粒细胞明胶酶相关脂质运载蛋白（NGAL）表达增加，诱导了大鼠肾毒性模型[9]。