Intervention of selenium on neurogranin expression in filial cerebrum of mice with excess iodine / 中华预防医学杂志

<p><b>OBJECTIVE</b>To study the effects of excess iodine intake on neurogranin expression in cerebrum of filial mice and the intervention of selenium.</p><p><b>METHODS</b>Sixty BALB/c mice were divided randomly into four groups with different drinking water: control group (tap water, NC), excess iodine group (3000 microg/L I, EL +), supplementing selenium group (200 microg/L Se, Se +) and the excess iodine plus selenium (3000 microg/L + I 200 microg/L Se, EI + Se +) group. The mice were mated at the end of the fourth month. Serum T4 and T3 were determined on postnatal day 14 and 28. The expression level of neurogranin in filial cerebrum was measured by immunohistochemistry and Western blot.</p><p><b>RESULTS</b>Serum T4 level in EI (68.78 +/- 11.10 nmol/ L) + was lower significantly than that in NC (100.85 +/- 11.47 nmol/ L) and EI + Se + (93.15 +/- 12.10 nmol/ L) on postnatal day 14. Western blot analysis showed that the relative level of neurogranin in EI + (0.621 +/- 0.041) was lower than that in NC (0.841 +/- 0.039) and EI + Se + (0.781 +/- 0.029) on postnatal day 14 (P < 0.05). No significant difference in serum T4 and neurogranin level between four groups on postnatal day 28.</p><p><b>CONCLUSION</b>Excess iodine intake might change the expression of neurogranin in filial cerebrum and the selenium supplementation might alleviate it.</p>

Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities.</p><p><b>METHODS</b>Weanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined.</p><p><b>RESULTS</b>Excessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression.</p><p><b>CONCLUSION</b>Relative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.</p>

ROS-related enzyme expressions in endothelial cells regulated by tea polyphenols / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Elevation of reactive oxygen species (ROS), especially the level of superoxide is a key event in many forms of cardiovascular diseases. To study the mechanism of tea polyphenols against cardiovascular diseases, we observed the expressions of ROS-related enzymes in endothelial cells.</p><p><b>METHODS</b>Tea polyphenols were co-incubated with bovine carotid artery endothelial cells (BCAECs) in vitro and intracellular NADPH oxidase subunits p22phox and p67phox, SOD-1, and catalase protein were detected using Western blot method.</p><p><b>RESULTS</b>Tea polyphenols of 0.4 microg/mL and 4.0 microg/mL (from either green tea or black tea) down-regulated NADPH oxidase p22phox and p67phox expressions in a dose-negative manner (P < 0.05), and up-regulated the expressions of catalase (P < 0.05).</p><p><b>CONCLUSIONS</b>Tea polyphenols regulate the enzymes involved in ROS production and elimination in endothelial cells, and may be beneficial to the prevention of endothelial cell dysfunction and the development of cardiovascular diseases.</p>

Induction of heme oxygenase-1 in human hepatocytes to protect them from ethanol-induced cytotoxicity / 生物医学与环境科学（英文）

<p><b>UNLABELLED</b>We investigated the relationship between ethanol exposure and heme oxygenase (HO-1) in human hepatocytes in order to ascertain if induction of HO-1 can prevent ethanol induced cellular damage.</p><p><b>METHODS</b>Dose-dependent (25-100 mmol/L) and time-dependent (0-24 h) ethanol exposure were used in the present study. HO-1 mRNA and protein expression were detected by PT-PCR and Western blot respectively. HO-1 activity was indicated by bilirubin and Fe2+ formation. Cytotoxicity was investigated by means of lactate dehydrogenate (LDH) and aspartate transaminase (AST) level in culture supernatants, as well as the intracellular formation of malondialdehyde (MDA), cellular glutathione (GSH) status and CYP 2E1 activity.</p><p><b>RESULTS</b>We first demonstrated a dose-dependent response between ethanol exposure and HO-1 mRNA and protein expression in human hepatocytes. We further observed a time-dependent increase of HO-1 mRNA expression using 100 mmol/L ethanol starting 30 minutes after ethanol exposure, reaching its maximum between 3 h and 9 h. Being similar increased protein expression started to what had been demonstrated with the mRNA level, at 6 h after ethanol exposure, and kept continuous elevated over 18 h. In addition, we found that ethanol exposure to hepatocytes markedly increased HO-1 enzyme activity in a time-dependent manner measured as bilirubin and Fe2+ formation in human hepatocytes. Our results clearly showed that ethanol exposure caused a significant increase of LDH, AST, and MDA levels, while the antioxidant GSH was time-dependently reduced. Furthermore, we demonstrated that pre-administration of cobalt protoporphyrin (CoPP) induced HO-1 in human hepatocytes, and prevented an increase of MDA and a decrease of GSH. These effects could be partially reversed by zinc protoporphyrin (ZnPP), an antagonist of HO-1 induction.</p><p><b>CONCLUSION</b>HO-1 expression in cells or organs could lead to new strategies for better prevention and treatment of ethanol-induced oxidative damage in human liver.</p>

Influence of alcohol on insulin sensitivity and insulin receptor substrate-1 mRNA expression in rat skeletal muscle / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate the molecular mechanism of the effect of alcohol on insulin sensitivity.</p><p><b>METHODS</b>Four groups of Wistar rats were used, i.e. control (C) group, and low (L), moderate (M) and high (H) alcohol group. Alcohol doses of each group were 0, 0.6, 1.8 and 3.0 ml.(kg.bw)(-1).day(-1). Each group was comprised of 10 male and 10 female rats. Alcohol was given to rats by gastric intubation. Thirteen weeks later, serum was collected for testing of fasting plasma glucose and insulin. HOMA-IR index of each group were calculated. Total muscle RNA was extracted using Trizol Reagent (Promega). The expression level of IRS-1 mRNA in muscle was detected by RT-PCR.</p><p><b>RESULTS</b>In female rats, the fasting plasma glucose of group (8.36 +/- 0.57) mmol/L was higher and the fasting plasma insulin (15.25 +/- 3.32) was lower than those of group C (7.56 +/- 0.85, 20.80 +/- 3.25). The HOMA-IR of group L (1.775 3 +/- 0.138 1) was lower than that of group C (1.982 6 +/- 0.124 6) (P < 0.05), while IRS-1 mRNA (0.766 1 +/- 0.076 9) was up-regulated (P < 0.05); HOMA-IR of group M (2.202 2 +/- 0.271 0) was higher than that of group C (P < 0.01), while IRS-1 mRNA (0.501 8 +/- 0.049 2) was suppressed (P < 0.01); HOMA-IR of group H (1.850 1 +/- 0.162 8) was not significantly changed as compared with that of group C (1.982 6 +/- 0.124 6) (P > 0.05), while IRS-1 mRNA (0.418 1 +/- 0.049 1) was significantly suppressed (P < 0.01). In male rats, the fasting plasma glucose and insulin had the similar change as those of female rats. The HOMA-IR of group M (1.878 5 +/- 0.250 2) was lower than that of C group (2.147 3 +/- 0.330 8) (P < 0.05), IRS-1 mRNA was up-regulated (0.824 9 +/- 0.064 7) (P < 0.05).</p><p><b>CONCLUSIONS</b>The present study showed that low-to-moderate dose of alcohol could increase insulin sensitivity; while alcohol abuse could decrease insulin sensitivity. Sex difference in this effect was found. Changes of IRS-1 mRNA expression may be involved in the molecular mechanism of the effects of alcohol on insulin sensitivity.</p>

Effects of long-term excessive Iodine intake on the maternal-fetal thyroid hormone metabolism in mice / 中华内分泌代谢杂志

Long-term excessive iodine intake resulted in an increased TT_4 level and a decreased TT_3 level in maternal serum,meanwhile,hepatic and renal type 1 deiodinase activity decreased dose-dependently.A significant reduction in type 2 deiodinase ( D2 ) activity of 12.5 d placenta was found in 3.0 mg/L or above groups.For 19.5 d uterus,D2 activity decreased and type 3 deiodinase activity increased.The results suggest that excessive iodine has an effect on the embryonic development by regulating maternal-fetal thyroid hormone metabolism.