FeTPPS is a metalloporphyrin-based ONOO⁻ decomposition catalyst [1]. FeTPPS catalyzes the decomposition of peroxynitrite (ONOO⁻), reducing its nitrating/oxidative damage to proteins, DNA, and lipids [2-3]. FeTPPS is primarily used in the study of oxidative stress-related disease models [4].
In cardiomyocytes, FeTPPS (50μM; 24h) reduces cell death caused by SIN-1 and SIN-1 plus H2O2 [5]. In spermatids, exposure to FeTPPS (25-50μM; 24h) ameliorates nitrosative stress [6].
In controlled cortical impact injury (CCI) mice model, FeTPPS (10mg/kg, 30mg/kg; ip; two injections) reduces secondary damage and improves neurobehavioral functions after traumatic brain injury. [7]. In a high-fat diet mice model, FeTPPS (50-60mg/kg; po; 8 weeks) treatment more than doubled the insulin-induced drop in blood glucose levels [8].
References:
[1]. Haber A, Gross Z. Catalytic antioxidant therapy by metallodrugs: lessons from metallocorroles[J]. Chemical Communications, 2015, 51(27): 5812-5827.
[2]. Uribe P, Barra J, Painen K, et al. FeTPPS, a Peroxynitrite Decomposition Catalyst, Ameliorates Nitrosative Stress in Human Spermatozoa[J]. Antioxidants, 2023, 12(6): 1272.
[3]. Zhang P, Ma L, Yang Z, et al. 5, 10, 15, 20-Tetrakis (4-sulfonatophenyl) porphyrinato iron (III) chloride (FeTPPS), a peroxynitrite decomposition catalyst, catalyzes protein tyrosine nitration in the presence of hydrogen peroxide and nitrite[J]. Journal of Inorganic Biochemistry, 2018, 183: 9-17.
[4]. Duan X, Wen Z, Shen H, et al. Intracerebral hemorrhage, oxidative stress, and antioxidant therapy[J]. Oxidative medicine and cellular longevity, 2016, 2016(1): 1203285.
[5]. Klassen S S, Rabkin S W. The metalloporphyrin FeTPPS but not by cyclosporin A antagonizes the interaction of peroxynitrate and hydrogen peroxide on cardiomyocyte cell death[J]. Naunyn-Schmiedeberg's archives of pharmacology, 2009, 379(2): 149-161.
[6]. Uribe P, Barra J, Painen K, et al. FeTPPS, a Peroxynitrite Decomposition Catalyst, Ameliorates Nitrosative Stress in Human Spermatozoa[J]. Antioxidants, 2023, 12(6): 1272.
[7]. Bruschetta G, Impellizzeri D, Campolo M, et al. FeTPPS reduces secondary damage and improves neurobehavioral functions after traumatic brain injury[J]. Frontiers in Neuroscience, 2017, 11: 6.
[8]. Duplain H, Sartori C, Dessen P, et al. Stimulation of peroxynitrite catalysis improves insulin sensitivity in high fat diet‐fed mice[J]. The Journal of physiology, 2008, 586(16): 4011-4016.
FeTPPS是一种基于金属卟啉的ONOO⁻分解催化剂 [1]。FeTPPS能催化过氧亚硝酸盐（ONOO⁻）的分解，从而降低其对蛋白质、DNA和脂质的硝化/氧化损伤 [2-3]。FeTPPS主要用于氧化应激相关疾病模型的研究 [4]。
在心肌细胞中，FeTPPS（50μM；24h）可减少SIN-1以及SIN-1与H2O2联合作用引起的细胞死亡 [5]。在精子细胞中，暴露于FeTPPS（25-50μM；24h）可改善亚硝化应激 [6]。
在受控皮质撞击损伤（CCI）小鼠模型中，FeTPPS（10mg/kg，30mg/kg；ip；两次注射）可减少脑外伤后的继发性损伤并改善神经行为功能 [7]。在高脂饮食小鼠模型中，FeTPPS（50-60mg/kg；po；8周）治疗使胰岛素引起的血糖水平下降幅度增加了一倍以上 [8]。