AC1及AC3抗白内障形成中晶状体谷胱甘肽代谢相关酶活性的变化

观察了亚硒酸钠,AC1,AC3对大鼠晶状体中谷胱甘肽过氧化物酶(GSH-Px),谷胱甘肽还原酶(GR)及谷胱甘肽硫转移酶(GST)的影响。结果表明,亚硒酸钠组大鼠的晶状体尚未混浊前已出现GSH-Px活性增高及GR和GST的活性降低。GR活性下降随白内障进展而加重。AC1及AC3均可使亚硒酸钠所致的酶活性变化逆转,但对正常晶状体的酶活性没有影响。     

Selenium in the anterior pituitary of the rat after a single injection of75Se sodium selenite

In order to investigate the selenite metabolism in the anterior pituitary and compare it with other endocrine organs, rats were injected intraperitoneally with⁷⁵Se sodium selenite (5 mg/kg). The rats were whole body counted shortly after injection and recounted just before sacrifice, which was performed 2, 24, 48 h, and 4, 10, 20, 30, 40, 60, and 80 d after injection. Besides the anterior pituitary, the selenium content was also estimated in the thyroid gland, testis, adrenals, liver, kidney, and blood. The maximum selenium content was observed in all organs 2 h after injection, at which time the anterior pituitary contained 2.9 μg/g wet wt, compared to 13.5 μ/g wet wt in liver and .6 μg/mg wet wt in testis. The excretion of selenite from the anterior pituitary resembled that seen in most other organs investigated, i.e., an initial rapid excretion and a slower secondary phase resembling a first order reaction. Practically all selenium was excreted by 60 d after injection.     

Production and detoxification of H2O2 in lettuce plants exposed to selenium

Selenium is considered an essential element for animals. Despite that it has not been demonstrated to be essential for higher plants, it has been attributed with a protective role against reactive oxygen species in plants subjected to stress. In this study, lettuce plants ( Lactuca sativa cv. Philipus) received different application rates (5, 10, 20, 40, 60, 80 and 120 μM) of selenite or selenate, with the aim of testing the effect of Se on the production and detoxification of H₂O₂ in non-stressed plants. The results indicate that the form selenate is less toxic than selenite; that is, the plants tolerated and responded positively to this element, and even increasing in growth up to a rate of 40 μM for the form selenate. On the contrary, the application of selenite triggered a higher foliar concentration of H₂O₂ and a higher induction of lipid peroxidation [malondialdehyde content and lipoxygenase activity] in comparison to that observed after the selenate application. Also, the plants treated with selenate induced higher increases in enzymes that detoxify H₂O₂, especially ascorbate peroxidase and glutathione (GSH) peroxidase, as well as an increase in the foliar concentration of antioxidant compounds such as ascorbate and GSH. These data indicate that an application of selenate at low rates can be used to prevent the induction in plants of the antioxidant system, thereby improving stress resistance.     

Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells

Introduction  In this study, we delineated the apoptotic signaling pathways activated by sodium selenite in NB4 cells. Materials and methods  NB4 cells were treated with 20 μM sodium selenite for different times. The activation of caspases and ER stress markers, ROS levels, mitochondrial membrane potential and cell apoptosis induced by sodium selenite were analyzed by immunoblotting analysis, DCF fluorescence and flow cytometric respectively. siRNA was used to detect the effect of GADD153 on selenite-induced cell apoptosis. Conclusions  Sodium selenite-induced reactive oxygen species generation is an early event that triggers endoplasmic reticulum stress mitochondrial apoptotic pathways in NB4 cells.     

Sodium selenite,dietary micronutrient,prevents the lymphocyte DNA damage induced by N-nitrosodiethylamine and phenobarbital promoted experimental hepatocarcinogenesis

Selenium (Se), a micronutrient, has a long history in chemoprevention of mammary and colon cancers in rodent models. Se is a current clinical trial, having shown promise in prevention of prostate and other human cancers. The mechanisms involved in the in vivo anti-carcinogenic activity of Se remain to be elucidated. In the present study, we examined the effect of sodium selenite supplementation in lymphocytes, obtained from hepatoma bearing rats on DNA damage in correlation with oxidative stress. In addition, this study examined the supplementation of Se at 4-ppm levels in the form of sodium selenite either before initiation or during initiation and/or promotion phase's increases lymphocyte Se concentrations. This in turn improves lymphocyte resistance to oxidative stress and protection against the lymphocytes DNA damage. Supplementation of Se increased lymphocyte Se concentration and reduced lymphocytes DNA damage as determined by single cell gel electrophoresis. The enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase, and catalase were found to be decreased while the thiobarbituric acid reactive substances level was increased in the lymphocytes of hepatoma bearing rats. Furthermore, the reactive oxygen species such as superoxide radicals and hydroxyl radicals were also found to be high in lymphocytes. Our present results explain the understanding of unique association between anti-peroxidative effect of Se and ultimately the capability of Se to prevent cancer.     

Screening yeast cells for absorption of selenium oxyanions

Certain yeast cells on solid nutrient medium produced colonies surrounded by a light zone of selenite absorption. This screening procedure resulted in the selection of 22 strains out of 200 isolates with different Se⁴⁺-absorbing capacity ranging from 16 to 98.8 g Se⁴⁺ g^–1 l^–1 h^–1. The highest rate of Se⁴⁺ elimination from the Na₂SeO₃ solution was observed with an oval shaped, cream pigmented fermentative yeast, tentatively called Candida sp. strain MS4. This strain was isolated from wastewater and found to accumulate selenium oxyanions. Se⁴⁺ uptake involved both inactive and active phenomena. The amounts of selenium (initial concentration 2 mg Se⁴⁺ l^–1) removed from aqueous solution by inactive and active phenomena were 667 g Se⁴⁺ g^–1 l^–1, and 1580 g Se⁴⁺ g^–1 l^–1, respectively. The strain also removed selenate inactively (135 g Se⁶⁺ g^–1 l^–1).     

Selenium protects cerebral ischemia in rat brain mitochondria

Normal cellular metabolism produces oxidants that are neutralized by the cells' antioxidant enzymes and antioxidants taken from outside. An imbalance between oxidant and antioxidant has been postulated to lead to the neurodegeneration in the ischemic condition. In this study, we have demonstrated the prevention or slowdown of neuronal injury in middle cerebral artery occlusion (MCAO) by sodium selenite. Rats were pretreated with 0.05, 0.1, and 0.2 mg/kg body wt of sodium selenite for 7 d. The rats of group I (sham) and group II (ischemia) were pretreated with physiological saline for 7 d. On d 8, MCAO was induced for 2 h in, the right side of brain of group II, III, IV, and V rats. Brains were dissect out after 22 h of reperfusion and washed with chilled physiological saline. The right cerebral hemisphere was used for the preparation of mitochondria. The activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and monoamine oxidase (MAO-A and MAO-B) was depleted significantly; conversely, the activity of poly(ADP-ribosyl) polymerase was elevated significantly as compared to the sham, and the pretreatment of the animals with different doses of sodium selenite has protected the activity of these enzymes significantly. The content of glutathione was decreased significantly, whereas the level of lipid peroxidation was increased significantly in the mitochondria of MCAO as compared to the sham group, and pretreatment with different doses of sodium selenite has protected their levels significantly as compared to the MCAO group. It is concluded that selenium, which is an essential part of our diet, might be helpful in protection against neurodegeneration in cerebral ischemia.     

Protective effect of selenium treatment on diabetes-induced myocardial structural alterations

One of the main causes leading to mortality in diabetes is myocardial disease. Using streptozotocin (STZ)-induced diabetic animals, it has been possible to characterize diabetes-induced myocardial abnormalities. Interstitial and microvascular disorders are known to be a characteristic part of the diabetic cardiomyopathy and partly resist insulin therapy. Because diabetic damage is partly attributed to oxidative stress, antioxidant treatment may be able to reduce this damage. The aim of this study was to investigate the cardioprotective effect of sodium selenite, known as an antioxidant agent. The diabetes was induced by ip injection of 50 mg/kg body wt STZ. The duration of diabetes was 5 wk. The protected group received (ip) 5 μmol/kg body wt/d sodium selenite (Na₂SeO₃) over 4 wk following diabetes induction. Electron and light microscopic morphometry of heart samples revealed typical diabetic alterations consisting in an increase in collagen content, vacuolation, diminishing of the cardiomyocyte diameter, alteration in myofilaments and Z-lines of myofibers, and myofibrillary degeneration. Sodium selenite treatment could prevent the loss of myofibrills and reduction of myocyte diameter. In the sodium-selenite-treated diabetic rat heart, alterations of the discus intercalaris and nucleus were corrected, and degenerations seen in myofilaments and Z-lines were reversed by this treatment. Under these findings, one can suggest that sodium selenite treatment may alleviate late diabetic complications when it is used under control conditions.     

Toxic concentrations of selenite shortens repolarization phase of action potential in rat papillary muscle

Selenium (Se) has long been recognized as both an essential mammalian nutrient and a hazardous element. Sodium selenite is commonly used as a dietary supplement for the treatment of Se deficiency. On the other hand, chronic Se toxicity has been demonstrated to affect the major organs, including the heart, in experimental animals. This study examines the effects of high concentrations of extracellular selenite (in the range of 0.001–1 mM) application into the recording bath on the electrical properties of rat papillary muscles. Conventional glass semifloating microelectrodes were used to record intracellular action potentials (APs) in isolated rat papillary muscles. The amplitude of APs and the resting membrane potential of papillary muscles were not changed following a 20-min selenite (1 mM) application compared to the first minute of its application. Freshly isolated ventricular myocytes by an enzymatic method were used to determine the selenite-induced alterations in Na⁺ currents. Na⁺ currents, measured at 22°C, by the whole-cell patch-clamp technique, decreased by 38±8% in the presence of 1 mM selenite for 5 min. These selenite-induced effects were not reversed, but are restored by dithiothreitol (1 mM). These results demonstrated that toxic concentrations of selenite induced a significant shortening in AP duration as a result of an increase in the rate of repolarization. Our findings also suggest that a decrease in Na⁺ currents, in addition to Ca²⁺ currents, may play a role in the shortening of AP duration in rat papillary muscles.