Effect of Dietary Vitamin C on the Antioxidant Defense System of Hibernating Juvenile Three-keeled Pond Turtles (Chinemys reevesii)

Juvenile three-keeled pond turtles(Chinemys reevesii) were fed diets supplemented with vitamin C(Vc) at doses of 0(basal diet, Vc0), 100(Vc100), 200(Vc200), 500(Vc500) and 2500(Vc2500) mg/kg diets at 28°C for 4 weeks, respectively. Then, the water temperature was gradually reduced to 10°C, and the turtles were induced into hibernation. Liver tissue samples were collected at three time points: start of hibernation(T1), 4 and 6 weeks’ hibernation(T2 and T3). A control group fed with the basal diet was set to parallel the whole treatment process, but reared at 28°C constantly. The results showed that hibernation mildly affected the antioxidant system and the influence varied with hibernating time. Hepatic malondialdehyde content of the Vc100 group was significantly lower than that of the other groups at T1. At T2, hepatic MDA in the groups of Vc500 and Vc2500 decreased significantly, while no clear differences were found among all groups at T3. The activities of antioxidant enzymes showed a positive correlation with dietary Vc dose before hibernation. After hibernation, total antioxidant capability was not affected by Vc. Superoxide dismutase activity became similar in different groups at T2, but decreased in higher Vc groups(≥ 200 mg/kg) at T3. Glutathione peroxidase and glutathione-S-transferase activities decreased significantly with dietary Vc supplementation(≥ 100 mg/kg) at T2, but recovered at T3. The result indicates that under normal rearing condition, low dietary Vc supplementation(< 100 mg/kg) might be beneficial to the antioxidant defense system. The effect of dietary Vc on the antioxidant defense system differed during hibernation.

Synthesis of two new thiazolidines and their hepatoprotective effects

Two new 2-substituted thiazolidine-4（R）-carboxylic acids （TCAs）, 2-glusosaminal-TCA （GIcNH2Cys） and 2-N-acetyl-glueosanlinal-TCA （GlcNAeCys）, were synthesized. Their protective effects against liver toxicity induced by acetaminophen （APAP） were investigated in a mice model. The resuits demonstrate that administration of TCAs （ i. p. , 800 mg/kg） 30 min after APAP challenge efficiently decrease ALF, AST, and LDH levels in liver. GlcNAcCys shows the best proteetive eftects, decreasing ALT, AST and LDH levels to 63%, 18.4% and 37% of the APAP group respectively. Comparison with the control showed that APAP greatly decreases total sulfhydlyl （T-SH） levels （43%）, non-protein hound sulfhydryl （NP-SH） levels （50%） and total antioxidative capabilities （57%） in the liver 24 hr after challenge. TCAs treatments 30min after APAP challenge significantly elevate sulfhydryl levels and total antioxidative capabilities. APAP administration also markedly （P 〈 0.05） increases liver lipid peroxidation to 1.65 and 1.17 times that of the control 4 hr and 24 hr after APAP administration respectively. TCAs treatments can inhibit lipid peroxidation as measured by decreased malondialdehyde （MDA） contents in liver. The histopathological results also further confirm the hepatoprotective effects of TCAs. In conclusion, our data show that TCAs, GleNAcCys particularly, have hepatoprotective anti antioxidant etfects.

Integrative analysis of the transcriptome and metabolome reveals the importance of hepatokine FGF21 in liver aging

Aging is a contributor to liver disease.Hence,the concept of liver aging has become prominent and has attracted considerable interest,but its underlying mechanism remains poorly understood.In our study,the internal mechanism of liver aging was explored via multi-omics analysis and molecular experiments to support future targeted therapy.An aged rat liver model was established with D-galactose,and two other senescent hepatocyte models were established by treating HepG2 cells with D-galactose and H2O2.We then performed transcriptomic and metabolomic assays of the aged liver model and transcriptome analyses of the senescent hepatocyte models.In livers,genes related to peroxisomes,fatty acid elongation,and fatty acid degradation exhibited down-regulated expression with aging,and the hepatokine Fgf21 expression was positively correlated with the down-regulation of these genes.In senescent hepatocytes,similar to the results found in aged livers,FGF21 expression was also decreased.Moreover,the expressions of cell cycle-related genes were significantly down-regulated,and the down-regulated gene E2F8 was the key cell cycle-regulating transcription factor.We then validated that FGF21 overexpression can protect against liver aging and that FGF21 can attenuate the declines in the antioxidant and regenerative capacities in the aging liver.We successfully validated the results from cellular and animal experiments using human liver and blood samples.Our study indicated that FGF21 is an important target for inhibiting liver aging and suggested that pharmacological prevention of the reduction in FGF21 expression due to aging may be used to treat liver aging-related diseases.

Antioxidation of Anthocyanins in Photosynthesis Under High Temperature Stress

Chlorophyll fluorescence and antioxidative capability in detached leaves of the wild type Arabidopsis thaliana L. ecotype Landsberg erecta （Ler） and three mutants deficient in anthocyanins biosynthesis （tt3, tt4, and tt3tt4） were investigated during treatment with temperatures ranging 25-45 ℃. In comparison with the wild type, chlorophyll fluorescence parameters Fv/Fm, φps,, electron transport rate （ETR）, Fv/Fo and qP in three anthocyanin-deficient mutants showed a more rapidly decreasing rate when the temperature was over 35 ℃. Non-photochemical quenching （NPQ） in these mutants was almost completely lost at 44 ℃, whereas the content of heat stable protein dropped and the rate of the membrane leakage increased. Fo-temperature curves were obtained by monitoring Fo levels with gradually elevated temperatures from 22 ℃ to 72 ℃ at 0.5 ℃/min. The inflexion temperatures of Fo were 45.8 ℃ in Ler, 45.1℃ in tt3, 44.1℃ in tt4 and 42.3 ℃ in tt3tt4, respectively. The temperatures of maximal Fo in three mutants were 1.9-3.8℃ lower than the wild type plants. Meanwhile, three mutants had lower activities of superoxide dismutase （SOD） and ascorbate peroxidase （APX） and an inferior scavenging capability to DPPH （1.1-diphenyl-2-picrylhy.drazyl） radical under heat stress, and in particular tt3tt4 had the lowest antioxidative potential. The results of the diaminobenzidine-H2O2 histochemical staining showed that H2O2 was accumulated in the leaf vein and mesophyll cells of mutants under treatment at 40 ℃, and it was significantly presented in leaf cells of tt3tt4. The sensitivity of Arabidopsis anthocyanins-deficient mutants to high temperatures has revealed that anthocyanins in normal plants might provide protection from high temperature injury, by enhancing its antioxidative capability under high temperature stress.