Inhibition of amino acid incorporation in a cell-free system and inhibition of protein synthesis in cultured cells by reaction products of selenite and thiols

Vernie, L.N.; Vries, M. De; Karreman, Leendert; Topp, Randolf J.; Bont, W.S.

doi:10.1016/0167-4781(83)90037-4

Cited by 24 publications

(7 citation statements)

References 16 publications

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“…Frenkel et al [65] have demonstrated that DNA polymerase a was inhibited by 1 pAf selenotrisulfide. This demonstration fits nicely with the observa tions of selenotrisulfide inhibition of protein synthesis [48,69] and cell growth [70], The data on the possible effects of selenotrisulfides on cell metabolism certainly warrant further investigation. Although there are se rious caveats to some of the other experi ments (see disussion on page 4), these path ways represent feasible mechanisms of sele nium action.…”

Section: Possible Mechanisms Of Selenium Actionsupporting

confidence: 58%

Current Ideas on Selenium as a Chemopreventive Agent

Medina

Morrison

1988

Path Immunopathol Res

102

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Section: Possible Mechanisms Of Selenium Actionsupporting

confidence: 58%

Current Ideas on Selenium as a Chemopreventive Agent

Medina

Morrison

1988

Path Immunopathol Res

102

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“…Even when the synthase is inhibited, sleep may be maintained by the PGD2 already present in the brain until it reaches a level too low to be effective. Some in vitro studies reported previously provide data suggesting that selenocompounds react with thiols such as glutathione and DTT to form products that in turn play a vital role in many metabolic reactions (17)(18)(19)(20). Islam et al (11) also showed in their in vitro study that small amounts of DTT were required for the inhibition of PGD synthase by selenocompounds.…”

Section: Discussionmentioning

confidence: 78%

“…4), but the minimal increase observed between 1300 and 1400 hr cannot explain the profound inhibition of SWS and PS during this period (Fig. 2) 20 (n = 4), 60 (n = 3), 100 (n = 4), 200 (n = 4), 400 (n = 5), and 600 (n = 5) pmol/0.2 ul per min. *, P < 0.05; **, P < 0.01; ***, P < 0.001 (by paired t test).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of sleep in rats by inorganic selenium compounds, inhibitors of prostaglandin D synthase.

Matsumura

Takahata

Hayaishi

1991

Proc. Natl. Acad. Sci. U.S.A.

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Prostaglandin (PG) D2 has been postulated to be an endogenous sleep-promoting factor in rats, and SeC14 and Na2SeO3 recently have been shown to inhibit the PGD synthase (prostaglandin-H2 D-isomerase, EC 5.3.99.2) activity of rat brain. The effect of these selenium compounds on sleep-wake activities was examined in freely moving rats along with their effects on brain temperature, food and water intake, and behavior. Test substances were administered for 6 hr into the third ventricle of rats, using a microdialysis technique. SeC4, time-and dose-dependently, inhibited sleep at perfusion rates of 60 pmol/0.2 jcl per min and higher, and the inhibition was almost complete at rates >200 pmol/0.2 gIl per min. The effect was reversible and was followed by a rebound. Na2SeO3 exhibited similar effects, but Na2SO3 did not show any effect on sleep. Simultaneous administration of dithiothreitol eliminated the sleep-inhibiting effects of these selenium compounds. These findings indicate that the decrease in sleep is due to inhibition of the PGD synthase activity in the brain by SeCL4 as-well as Na2SeO3. During the inhibition of sleep, the rats in general showed an activation of behavior with moderate elevation of brain temperature and a detectable increase in food and water intake, suggesting that the sleep-inhibited state of the rats was similar to the physiological state of wakefulness and that the inhibitory effect was not due to the general toxicity of selenium.Prostaglandins (PGs) D2 and E2, which are the major PGs in the brain of mammals, have been postulated to be endogenous factors for regulating sleep-wake activities in the rat and monkey (1, 2)-the former promoting sleep (3, 4) and the latter augmenting wakefulness (5-7). Naito et al. (8) reported the effects of intracerebroventricularly and systemically administered cyclooxygenase inhibitors such as indomethacin and diclofenac sodium on the sleep-wake activities of rats. However, these inhibitors are not specific for PG0)2 but prevent the synthesis of PGH2 from arachidonate, which in turn affects the consequent production of various eicosanoids, including PGD2 and E2. The rat brain PGD synthase (prostaglandin-H2 D-isomerase, EC 5.3.99.2) was purified to homogeneity and characterized by Urade et al. (9,10). More recently, Islam et al. (11) demonstrated in an in vitro study that inorganic quadrivalent selenocompounds, such as SeCL4 and Na2SeO3, inhibited the activity of the rat brain PGD synthase whereas other enzymes in the arachidonate cascade were not affected. Therefore, these selenocompounds may serve as useful probes for elucidating the role of endogenous PGD2 in the physiological sleep-wake regulation.In the present study, the effects of selenocompounds on sleep-wake activities, brain temperature, food and water intake, and behavior were examined in freely moving rats by administration of these compounds into the third ventricle via a microdialysis probe. The results obtained add further support to the hypothesis that PGD2 is involved in the promotion ...

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“…found that reduction in selenite by GSH into selenide resulted in superoxide (

O_{2}^{-}

) formation and suggested the latter to be the cytotoxic cause of selenium‐induced cell death. It has further been shown that addition of reduced extracellular GSH together with selenite increases the selenium uptake and cytotoxicity, leading to a decrease in intracellular GSH and an increase in the consumption of oxygen .…”

Section: Targeting Redox Regulation In Cancer Cells By Selenium Compomentioning

confidence: 99%

Selenium Cytotoxicity in Cancer

Wallenberg

Misra

Björnstedt

2014

Basic Clin Pharma Tox

107

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Selenium is an essential trace element with growth-modulating properties. Decades of research clearly demonstrate that selenium compounds inhibit the growth of malignant cells in diverse experimental model systems. However, the growth-modulating and cytotoxic mechanisms are diverse and far from clear. Lately, a remarkable tumour selective cytotoxicity of selenium compounds has been shown, indicating the potential of selenium in the treatment of cancer. Of particular interest are the redoxactive selenium compounds exhibiting cytotoxic potential to tumour cells. These selenium compounds elicit complex patterns of pharmacodynamics and pharmacokinetics, leading to cell death pathways that differ among compounds. Modern oncology often focuses on targeted ligand-based therapeutic strategies that are specific to their molecular targets. These drugs are initially efficient, but the tumour cells often rapidly develop resistance against these drugs. In contrast, certain redox-active selenium compounds induce complex cascades of pro-death signalling at pharmacological concentrations with superior tumour specificity. The target molecules are often the ones that are important for the survival of cancer cells and often implicated in drug resistance. Therefore, the chemotherapeutic applications of selenium offer great possibilities of multi-target attacks on tumour cells. This MiniReview focuses on the tumour-specific cytotoxic effects of selenium, with special emphasis on cascades of cellular events induced by the major groups of pharmacologically active selenium compounds. Furthermore, the great pharmacological potential of selenium in the treatment of resistant cancers is discussed.

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Inhibition of amino acid incorporation in a cell-free system and inhibition of protein synthesis in cultured cells by reaction products of selenite and thiols

Cited by 24 publications

References 16 publications

Current Ideas on Selenium as a Chemopreventive Agent

Current Ideas on Selenium as a Chemopreventive Agent

Inhibition of sleep in rats by inorganic selenium compounds, inhibitors of prostaglandin D synthase.

Selenium Cytotoxicity in Cancer

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