This study was conducted to compare the antioxidant, anticytotoxic, and anti-inflammatory properties of Euphorbia maculata ethanol extract with those of E. supina ethanol extract. 2,2-Diphenyl-1-picrylhydrazyl (DPPH) radical and superoxide scavenging activities of E. maculata at 50 μg/mL were 38.3 ± 3.7 and 21.5 ± 1.2%, respectively, whereas those of E. supina at the same concentration were 109.4 ± 0.9 and 59.5 ± 4.8%, respectively. Oxygen radical absorbance capacities of E. maculata and E. supina at 10 μg/mL were 14.70 ± 0.63 and 26.17 ± 1.36 nmol/mL Trolox, respectively. Cupric reducing antioxidant capacities of E. maculata and E. supina at 10 μg/mL were 10.22 ± 0.97 and 62.99 ± 5.28 nmol/mL Trolox, respectively. Total phenolic contents of E. maculata and E. supina at 50 μg/mL were 29.03 ± 0.14 and 87.89 ± 0.20 nmol/mL gallic acid, respectively. E. maculata and E. supina were reported to prevent supercoiled DNA breakage induced by peroxyl and hydroxyl radicals in a concentration-dependent manner, where protection against the supercoiled DNA breakage provided by E. supina was greater than that provided by E. maculata. E. maculata and E. supina at 100 μg/mL inhibited tert-butyl hydroperoxide-induced cytotoxicity in HepG2 cells by 49.4 ± 4.3 and 87.3 ± 4.5%, respectively. E. maculata and E. supina at 500 μg/mL inhibited lipopolysaccharide-induced nitric oxide production in RAW 264.7 cells by 63.1 ± 7.0 and 85.2 ± 1.6%, respectively. The antioxidant capacities including DPPH radical scavenging, superoxide scavenging, oxygen radical absorbance, and cupric reducing antioxidant activity were found to be highly correlated with total phenolic content (0.896 < r < 0.983, p < 0.01) and anticytotoxic activities (0.915 < r < 0.960, p < 0.01). However, the superoxide scavenging activity was not significantly correlated (r = 0.604, p > 0.05) with the anti-inflammatory activity. Thus, these findings demonstrated that the radical scavenging, anticytotoxic, and anti-inflammatory capacities of E. supina were more potent than those of E. maculata. Further studies are needed to elucidate the properties of polyphenolic constituents in E. supina responsible for these effects and the underlying mechanisms.

The objective of this study was to investigate anticytotoxic and antioxidatative capacities of ethanol extracts from Acer tegmentosum Maxim (A. tegmentosum) stem in vitro. The extract at concentration of 200 ug/mL inhibited 10 and 20 ug/mL arsenic trioxide-induced cytotoxicity of HepG2 cells by 79.3 and 57.5%, respectively. The extract at concentration of 200 ug/mL inhibited 0.2 and 0.5 mM t-BHP-induced cytotoxicity of HepG2 cells by 66.3 and 35.7%, respectively. Antioxidative effects of the extract were examined via measurement of ABTS, superoxide, and peroxyl radical scavenging activities. ABTS radical scavenging activity of the extract was higher than that of α-tocopherol. Superoxide scavenging activity of the extract was higher than that of catechin. Oxygen radical absorbance capacity of the extract was higher than that of ascorbic acid. Cupric reducing antioxidant capacity of the extract was higher than that of α-tocopherol. The extract at concentrations of 100 and 500 μg/mL inhibited 10 mM t-BHP-induced lipid peroxidation of HepG2 cells by 38.2 and 80.7%, respectively. The extract prevented supercoiled DNA strand breakage induced by hydroxyl or peroxyl radical. Total phenolic and flavonoid contents of the extract at concentration of 100 μg/mL were 71.3 nmol/mL gallic acid and 18.8 nmol/mL catechin equivalents, respectively. Thus, strong cytoprotective and antioxidant effects of A. tegmentosum stem extract seem to be due to, at least in part, the prevention from free radicals-induced oxidation as well as high levels in polyphenolic contents.

The objective of present study was to investigate the anti oxidative and hepatoprotective effects of tomato extracts. Total antioxidant capacity and total antioxidant response were 5.5 and 19.8μg Trolox equivalent per mg of tomato extract, respectively. DPPH radical scavenging activity of tomato extracts (10mg ml-1) was 70% as compared to 100% by pyrogallol solution as a reference. The effect of the tomato extracts on lipid peroxidation was examined using rat liver mitochondria induced by iron/ascorbate. Tomato extracts at the concentration of 0.5mg ml-1 significantly decreased TBARS concentration. Tomato extracts prevented lipid peroxidation in a dose-dependent manner. The effect of the tomato extracts on reactive oxygen species (ROS) generation was examined using cell-free system induced by H2O2/FeSO4. Addition of 1mg ml-1 of tomato extracts significantly reduced dichlorofluorescein (DCF) fluorescence. Tomato extracts caused concentration-dependent attenuation of the increase in DCF fluorescence, indicating that tomato extracts significantly prevented ROS generation in vitro. The effect of tomato extracts on cell viability and proliferation was examined using hepatocyte culture. Primary cultures of rat hepatocytes were incubated with 1mM tert-butyl hydroperoxide (t-BHP) for 90 min in the presence or absence of tomato extracts. MTT values by addition of tomato extracts at the concentration of 2, 10, and 20mg ml-1 in the presence of t-BHP were 13, 33 and 48%, respectively, compared to 100% as control. Tomato extracts increased cell viability in a dose-dependent manner. These results demonstrate that tomato extracts suppressed lipid peroxidation and t-BHP-induced hepatotoxicity and scavenged ROS generation. Thus antioxidant and hepatoprotective effects of tomato extracts seem to be due to, at least in part, the prevention from free radicals-induced oxidation, followed by inhibition of lipid peroxidation.

The objectives of present study were to investigate the effects of benzo[a]pyrene(BaP) on cytotoxicity, lipid peroxidation and antioxidant enzymes in rat hepatocyte primary culture. Primary cultures of rat hepatocytes were incubated for 24 hr, 48 hr or 72 hr in the presence of various concentrations (0, 10, 20, 30, 50 or 100 μM) of BaP. Cytotoxicity and cell viability were determined by measuring glutamic oxaloacetic transaminase(GOT) activity, lactate dehydrogenase(LDH) activity and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) value. Lipid peroxidation was evaluated using thiobarbituric acid reactive substances(TBARS) assay. Effects on antioxidant system were determined by measuring glutathione peroxidase(GPx) activity, glutathione reductase(GR) activity and glutathione concentration. Activities of GOT and LDH, MTT value as well as TBARS concentration were not affected by up to 100 μM of BaP for 24 hr incubation. However, BaP at the concentration of 50 μM for 48 hr incubation or at the concentration of 30 μM for 72 hr incubation began to increase LDH activity and TBARS concentration but decrease MTT value, representing that BaP caused cytotoxicity and decreased cell viability in dose- and time-dependent manners. GPx activity began to be decreased by BaP at the concentration of 50 μM for 72 hr incubation. Whereas, GR activity began to be decreased by BaP at the concentration of 20 μM for 72 hr incubation. Glutathione concentration began to be decreased by BaP at the concentration of 20 μM for 72 hr incubation and was further reduced to 90% by 100 μM of BaP. These results demonstrate that BaP caused cytoctoxicity and decreased cell viability by increasing lipid peroxidation and decreasing glutathione concentration as well as activities of GPx and GR.