Objective: To study the effects of sodium selenite at large doses on selenoenzyme gene expression and activity in rat livers. Methods: Rats were injected intra-peritoneally (ip) with 0, 20, 40, and 80 ?g /(kg?d) Se of sodium selenite dissolved in 0.9% physiological saline for 15 days. Livers were sampled and partly used for histological study. The rests were homogenized for reverse transcription-polymerase chain reaction to semi-quantitatively detect differential gene expressions of glutathione peroxidase (GSH-Px) and thioredoxin reductase (TR) in livers. Meanwhile, selenoenzyme activities, Se contents and MDA levels were also measured. Results: Compared with the control group, the mRNA levels and enzyme activities of both GSH-Px and TR increased in rats supplemented with 20 ?g/(kg?d) selenite. However, the mRNA levels and activities of both selenoenzymes decreased significantly in rats injected with selenite at doses of 40 and 80 ?g /(kg?d) respectively (P

Object To investigate the antagonistic effect of scutellarin on the toxicity of selenium in human liver cells L-02. Methods MTT method was used to observe the effects of scutellarin and selenium on cell growth. The morphological changes of cells were observed by fluorescent microscope. The MDA level, thiol content, and total antioxidative capacity of cells were also measured. Results The optimum condition for scutellarin to promote cell growth was 0.5 mmol/L in 48 h culture period. Comparing with the only selenium treated group, 0.5 mmol/L scutellarin significantly antagonized the inhibition of cell growth caused by 1 and 5 ?mol/L selenium, suppressed the selenium-induced cell damage and the increase of MDA content, as well as increased the thiol content and cell antioxidation capacity. Conclusion Scutellarin markedly antagonizes the toxicity of selenium in human liver cells L-02 by inhibiting lipid peroxidation and promoting cellular antioxidation capacity.

AIM To explore the antagonistic effect of scutellarin on the liver toxicity of upper limit intake (UL) of Se. METHODS Chemical luminescence was used to determine the scavenging effect of scutellarin on reactive oxygen species (ROS) induced by Na 2SeO 3 in vitro . MDA content, the activities of SOD, CAT, GSH Px and histopathological sections were measured to investigate the effects of scutellarin on Se toxicity in rats. RESULTS In vitro experiment showed the ability of scutellarin to inhibit the generation of ROS effectively. MDA content was significantly decreased, the activities of SOD, CAT and GSH Px were significantly increased and liver injury was alleviated obviously in the UL Se plus scutellarin group as compared to the only UL Se group. CONCLUSION Scutellarin markedly antagonized the liver toxicity of UL Se through scavenging ROS induced by excess Se.

AIM To study the effects of Scutellarin on glutathione peroxidase and thioredoxin reductase gene expression and activities in liver, kidney and testis tissues of rats supplemented with upper limit intake (UL) of Se. METHODS RT PCR and enzyme activities were used to determine GSH Px and TR mRNA levels and activities. RESULTS GSH Px and TR mRNA levels and activities were remarkably decreased in livers of rats supplemented with UL Se. Scutellarin significantly increased GSH Px and TR mRNA levels and activities in livers of rats supplemented with UL Se. No significant effects were found in rats treated with only Scutellarin as compared with the control. There were also no significant effects of UL Se on GSH Px and TR mRNA levels and activities in rat kidney and testis. CONCLUSION Scutellarin effectively antagonized the decrease of GSH Px and TR mRNA levels and activities in rat livers due to supplementation with UL. The effect of UL on GSH Px and TR mRNA levels shows tissue specificity.