S-allylcysteine scavenges singlet oxygen and hypochlorous acid and protects LLC-PK1 cells of potassium dichromate-induced toxicity

It has been found that S-allylcysteine (SAC), a garlic-derived compound, has in vivo and in vitro   antioxidant properties. In addition, it is known that SAC is able to scavenge different reactive oxygen or nitrogen species including superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH), and peroxynitrite anion (ONOO−) although the IC5O values for each reactive species has not been calculated and the potential ability of SAC to scavenge singlet oxygen (1O2) and hypochlorous acid (HOCl) has not been explored. The purposes of this work was (a) to explore the potential ability of SAC to scavenge 1O2 and HOCl, (b) to further characterize the O2-, H2O2, OH, and ONOO− scavenging ability of SAC by measuring the IC50 values using in vitro assays, and (c) to explore the potential ability of SAC to ameliorate the potassium dichromate (K2Cr2O7)-induced cytotoxicity in LLC-PK1 cells in which oxidative stress is involved. The scavenging activity was compared against the following reference compounds: N  -acetylcysteine for O2-, sodium pyruvate for H2O2, dimethylthiourea for OH, lipoic acid and glutathione for 1O2, lipoic acid for HOCl, and penicillamine for ONOO−. It was found that SAC was able to scavenge concentration-dependently all the species assayed with the following IC5O (mean ± SEM, mM): O2- (14.49 ± 1.67), H2O2 (68 ± 1.92), OH (0.68 ± 0.06), 1O2 (1.93 ± 0.27), HOCl (2.86 ± 0.15), and ONOO− (0.80 ± 0.05). When the ability of SAC to scavenge these species was compared to those of the reference compounds it was found that the efficacy of SAC (a) to scavenge O2-, H2O2, OH, and ONOO− was lower, (b) to scavenge HOCl was similar, and (c) to scavenge 1O2 was higher. In addition, it was found that SAC was able to prevent K2Cr2O7-induced toxicity in LLC-PK1 cells in culture. It was showed for the first time that SAC is able to scavenge 1O2 and HOCl and to ameliorate the K2Cr2O7-induced toxicity.