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Objective To study the effect of lipid peroxidation and anti-lipid peroxidation and the pigment in skin of C57BL/6 mice exposed to arsenic.Methods Forty male C57BL/6 mice were divided into four groups via the random number table method,ten mice in each group,and the mice were fed ad libitum drinking water containing arsenic at 0,1,5 and 25 mg/L concentrations for a period of 6 weeks,respectively.Twelve days before the end of the experiment,procedure of depilation was performed to induce anagen of hair cycle.On the 30th day of experiment,the activity of superoxide dismutase (SOD) was determined by nitrite method,the activity of glutathione peroxidase (GSH-Px) was determined by dithiobisobenzoic acid method,the content of malondialdehyde (MDA) in skin of C57BL/6 mice was determined by thiobarbituric acid method.Melanin was measured by NaOH dissolution method.Results No significant difference was found in body weight and water intaken between groups (F =0.119,0.363,P ＞ 0.05).The activity of SOD [(16.00 ± 5.05),(13.96 ± 2.02),(10.46 ± 3.14) U/mg prot] in 1,5 and 25 mg/L arsenic groups were all significantly lower than that in control group [(20.36 ± 4.82) U/mg prot,P ＜ 0.05].GSH-Px activity in 1,5 and 25 mg/L arsenic groups [(98.14 ± 23.92),(87.18 ± 10.87),(53.56 ± 19.97) U/mg prot] were all significantly lower than that in control group [(119.34 ± 33.14) U/mg prot,P ＜ 0.05].While MDA levels in 5 and 25 mg/L arsenic groups [(9.09 ± 2.04),(11.48 ± 2.21) nmol/mg prot] were significantly higher than that of control group [(6.19 ± 0.56) nmol/mg prot,P ＜ 0.05] and that of 1 mg/L arsenic group [(6.52 ± 1.67) nmol/mg prot,P ＜ 0.05).No significant difference was found in melanin levels (P ＞ 0.05).Conclusions Lipid peroxidation and the decreasing of antioxidation may be one of the mechanisms of arsenic-induced skin damage.Arsenic-induced skin melanin content change is not found.
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Antioxidant activity and total phenolic content of tamarind seed coat extracts (TSCEs) were compared between the two extracts using boiling-water (TSCE-W) and 70% ethanol (TSCE-E) for extraction. TSCE-W, consisting of the highest phenolic content, possessed 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging and anti-lipid peroxidation activities much higher than TSCE-E and Trolox. Additionally, both TSCEs also exhibited superoxide anion and hydrogen peroxide scavenging activities higher than Trolox and BHA. Anti-lipid peroxidation and cytotoxicity of TSCE-W were also studied in human foreskin fibroblast CCD-1064Sk cells. Cytotoxic effect was not observed when exposed to TSCE-W up to 1 mg/mL for 12-48 h. However, TSCE-W significantly attenuated lipid peroxidation in H2O2-damaged cells. HPLC analysis showed the presence of (+)-catechin, (-)-epicatechin, and procyanidin B2 in TSCE-W, which could be responsible for antioxidant and anti-lipid peroxidation activities. The results suggest that an inexpensive and simple boiling-water extraction of TSCE-W may provide a valuable natural antioxidant source having anti-lipid peroxidation for health food additives, nutraceuticals as well as cosmeceuticals.
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Objective To study on the anti-hepatic fibrosis effects of salvianolic acid A injection (SAA), and further to provide the theoretical basis for the clinical application .Methods Using CCl4 induced hepatocyte injury in vitro, the hepatocyte viability , the levels of ALT , AST and LDH in cell culture supernatants and the levels of SOD and MDA in cell lysates were detected .In addition , the hepatic fibrosis rat model was made by subcutaneous injection of CCl 4 , the serum LN, HA, SOD and MDA levels were detected and the pathological changes in liver tissue were also observed . Results Compared with model group , the hepatocyte viability in SAA high or low dose group and Vit E group were significantly increased (P <0.01), and the activities of ALT, AST and LDH in SAA high dose group were significantly lowed ( P <0.01 ) .The activity of SOD in SAA high dose group and Vit E group was significantly increased ( P <0.05), while MDA content was decreased (P <0.05).Vivo test showed that the levels of serum LN and HA in SAAhigh dose group were significant lower than those of hepatic fibrosis rat model group (P <0.05).Moreover, the activity of SOD in SAA high or low dose group was significantly increased (P <0.05, P <0.01), while MDA content was lowed (P <0.05, P <0.01), and can improve the pathological of liver tissues .Conclusions SAA injection can anti-lipid peroxidation and thereby protect hepatocyte and reduce hepatic fibrosis .
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Gold nanoparticles (Au-NPs) were synthesized from chloroauric acid using cell free supernatant of Streptomyces sp. NK52 grown in nutrient broth. These nanoparticles were synthesized by varying pH and temperature of the reaction mixture and chloroauric acid concentration. The nanoparticles were characterized by spectrometry, X-ray diffraction, Scanning electron microscopy and energy dispersive spectrometry. Au-NP ranged from 10-100 nm in size and exhibited a polydispersive nature with various shapes like rods, hexagons, triangles, spheres. The diffraction peaks at 2θ = 38.1◦ and 44.5◦ could be assigned to the (1 1 1) and (2 0 0) planes of a faced centre cubic (fcc) lattice of gold. Au-NP showed 47% inhibition of lipid peroxidation in vitro. To the best of our knowledge, this is the first report on the rapid biosynthesis of Au-NP using cell free supernatant of Streptomyces sp. and its evaluation for anti-lipid peroxidation.
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Cassia occidentalis Linn. mast cell degranulation at a dose of 250 mg/kg, showed dose dependent stabilizing activity towards human RBC, with is widely used in traditional medicine of India to treat a number of clinical conditions including allergy and inflammatory manifestations. In the present study anti-allergic, anti-inflammatory and anti-oxidant properties of C. occidentalis whole plant ethanolic extract (CO) was investigated. Effects of CO on rat mast cell degranulation inhibition and human red blood cell (HRBC) membrane stabilization were studied in vitro following standard methods. The anti lipidperoxidant effects of CO were also studied in vitro. Effect of CO on carrageenan-induced mouse paw oedema inhibition was also assessed. CO significantly decreased maximum protection of 80.8% at 15 μg/ml. The extract also caused significant reduction in malondialdehyde (MDA) levels of murine hepatic microsomes at 100 μg/ml (56%) and significantly reduced carrageenan induced inflammation in mice at a dose of 250 mg/kg. Results of the present study indicated that CO inhibited mast cell degranulation, stabilized HRBC membrane thereby alleviating immediate hypersensitivity besides showing anti oxidant activity.