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At least 19 recordsLinked to original sources
PubMed1978

Experimental studies on the intestinal uptake of organic and inorganic magnesium and potassium compounds given alone or simultaneously.

The peroral administration of magnesium and potassium compounds in effective doses (ED50) to rats yielded the following results: 1. Magnesium or potassium given as chlorides are significantly better absorbed than the corresponding aspartates. 2. In the presence of aspartate in higher concentrations the absorption of both magnesium and potassium is inhibited to a certain degree. 3. Increasing amounts of chloride cannot abolish the inhibitory effect of aspartate on potassium absorption, in contrast magnesium, which, in the presence of aspartate is better taken up when chloride is provided. 4. High concentrations of magnesium may perhaps impede the uptake of potassium to a small degree but not vice versa. 5. Magnesium losses from the body--induced by treatment with 9-alpha-fluorocortisol-acetate--can be effectively substituted by peroral administration of chloride-containing magnesium compounds over a reasonable time. The simultaneously occurring loss of potassium cannot be corrected correspondingly by potassium supplements.

Animals↗
PubMed1998

Powder Structure Solutions of the Compounds Potassium Phenoxide-Phenol: C(6)H(5)OK.xC(6)H(5)OH (x = 2, 3).

We report the ab initio structure solutions of two solvent containing potassium phenoxides by high-resolution powder X-ray diffraction. Both compounds are of interest for the classification of the mechanism of Kolbe-Schmitt type reactions. C(6)H(5)OK.2C(6)H(5)OH crystallizes in space group Abm2, Z = 4, with unit cell parameters a = 10.12458(4) Å, b = 21.2413(1) Å, c = 7.89784(3) Å. C(6)H(5)OK.3C(6)H(5)OH crystallizes in space group Pbca, Z = 8, with unit cell parameters a = 22.7713(1) Å, b = 25.4479(2) Å, c = 7.75549(4) Å. Both compounds show polymeric zigzag chains [K([6])O(2)([2])O([1])pi(phenyl)([1])] aligned along the c-axis. The coordination of the potassium ions is similar for both compounds. They lie at the center of distorted octahedra of five oxygen atoms and one phenyl ring, which donates its pi electrons. The distortion decreases as the number of free phenol increases.

Journal Article↗
PubMed1993

Growth of rho 0 human Namalwa cells lacking oxidative phosphorylation can be sustained by redox compounds potassium ferricyanide or coenzyme Q10 putatively acting through the plasma membrane oxidase.

Pyruvate is conventionally used as a key growth supplement for mammalian rho 0 cells that lack mitochondrial DNA and are thereby devoid of oxidative phosphorylation. We have tested the proposition that cultured rho 0 human cells can be grown using redox compounds other than pyruvate. The results show that potassium ferricyanide and coenzyme Q10 can each be used to replace pyruvate to support the growth of rho 0 Namalwa cells (a lymphoblastoid cell line). Ferricyanide and coenzyme Q10 have both been reported as substrates for a plasma membrane NADH oxidase system which is capable of re-oxidising cytosolic NADH to NAD+. These compounds are also known to stimulate the activity of this enzyme system. We interpret our data to indicate that redox support for growth of rho 0 human cells can be achieved by external electron acceptors such as ferricyanide (a plasma membrane impermeant compound), or coenzyme Q10 (an integral component of the plasma membrane oxidase), through the enhanced conversion of cytosolic NADH to NAD+. This re-oxidation of NADH enables glycolysis to function efficiently as the sole source of cellular ATP, in the absence of mitochondrial oxidative phosphorylation in rho 0 cells. This has important implications for the development of new strategies for the amelioration of the bioenergy decline that occurs in mitochondrial disease and during the human ageing process.

Cell Division↗
PubMed1990

Toxicity studies with potassium embelate, a new analgesic compound.

Potassium embelate, 2,5-dihydroxy, 3-undecyl-1, 4-benzoquinone, from Embelia ribes Burm. was subjected to toxicity evaluation which included subacute, chronic, reproductive toxicity testing and teratological investigations in laboratory animals (mice, rats and monkeys). The results did not indicate adverse effects suggesting that potassium embelate is a safe compound.

Abnormalities, Drug-Induced↗
PubMed1998

Effects of reducing, oxidizing and alkylating agents on early steps of Junin virus multiplication.

The action of reducing, oxidizing and thiol-alkylating agents on early steps of Junin virus (JV) multiplication in Vero cells was investigated. The presence of reducing agents during virus adsorption as well as incubation of viral particles with these compounds before infection enhanced JV infectivity. On the contrary, the thiol-alkylating agent 5,5' dithiobis (2-nitrobenzoic acid) and the oxidizing compound potassium periodate showed an inhibitory effect, suggesting that sulfhydryl groups, and certain sugar moieties of viral glycoproteins play an important role in the first steps of JV infection. Also enzymatic treatment of cell monolayers and addition of concanavalin A to cultures prior to infection suggest that cellular glycoproteins are involved in virus attachment.

Alkylating Agents↗
PubMed1999

[Plasmid DNA breakage caused by reaction of intracellular redox compound with potassium dichromate].

OBJECTIVE: To study plasmid DNA breakage induced by hexavalent chromium (Cr(VI +)) compound in vitro. METHODS: DNA breakage was observed using plasmid relaxation method. RESULTS: pUC 118 plasmid DNA single strand breakage can not be caused by either ascorbic acid (1 mmol/L), or glutathione (5 mmol/L), or hydrogen peroxide (H(2)O(2), 17 mmol/L) or potassium dichromate (K(2)Cr(2)O(7), 0.5 mmol/L) alone. But, if DNA was incubated warmly with K(2)Cr(2)O(7) and intracellular redox compound, pUC118 plasmid DNA single strand breakage could be induced by K(2)Cr(2)O(7), ascorbic acid, or glutathione, or products of peroxidation reaction. K(2)Cr(2)O(7) (0.5 mmol/L) and H(2)O(2) (17 mmol/L) also could cause some double-strand breakage in plasmid. CONCLUSION: It suggests that ascorbic acid, glutathione and H(2)O(2) can play an important role in carcinogenicity of K(2)Cr(2)O(7).

Antioxidants↗
PubMed1999

Genotoxic activity of different chromium compounds in larval cells of Drosophila melanogaster, as measured in the wing spot test.

Two chromium(VI) compounds (potassium chromate and potassium dichromate) and one chromium(III) compound, chromium chloride, were evaluated for genotoxic effects in the wing spot test of Drosophila melanogaster following standard procedures. This assay detects both somatic recombination and mutational events. The genotoxic effects were determined from the appearance of wing spots in flies transheterozygous for the third chromosome recessive markers multiple wing hairs (mwh) and flare-3 (flr(3)), as well as in flies heterozygous formwh and the multiply inverted TM3 balancer chromosome. Genetic changes induced in somatic cells of the wing's imaginal discs lead to the formation of mutant clones on the wingblade. Single spots are due to different genotoxic mechanisms: point mutation, deletion, chromosome breakage, and mitotic recombination; while twin spots are produced only by mitotic recombination. From our results it appears that both chromium(VI) compounds clearly increase the incidence of mutant clones by inducing high increases in the frequency of all types of clones recorded. On the contrary, chromium(III) did not increase the frequency of mutant clones. A high proportion of the total spot induction was due to mitotic recombination, confirming previously reported data on the strong recombinogenic activity of chromium(VI) compounds.

Animals↗
PubMed2003

Antigenotoxic properties of selenium compounds on potassium dichromate and hydrogen peroxide.

Selenium is an environmental metal that occurs ubiquitously and is produced throughout the world for various industrial activities. Selenium has been reported to have anticarcinogenic and preventive effects in clinical and epidemiological studies. Selenium supplements can inhibit chemically-induced tumours. From the viewpoint of genotoxicity, selenium has not been adequately studied and an IARC review concluded that there were not sufficient data to consider it a carcinogen for man. In contrast, hexavalent chromium is classified as a known respiratory carcinogen producing DNA damage through free oxygen radicals. In the present study, a collaborative study has been carried out to evaluate the genotoxicity of selenium compounds and their possible interactions with potassium dichromate and hydrogen peroxide. Thus, in laboratory 1 (U.K.), the genotoxic effects of three selenium compounds were examined. Sodium selenate, sodium selenite, and selenous acid were investigated in the Ames test using strain TA102 and in the Comet assay using human lymphocytes, and also investigated for their interaction with potassium dichromate. In the Ames test, it was shown that potassium dichromate produced a highly mutagenic response, whilst the three selenium compounds did not. In combination, sodium selenate reduced the genotoxicity of potassium dichromate, but sodium selenite and selenous acid had no effect. In the Comet assay, potassium dichromate induced DNA damage, but so did the selenium compounds. In combination with potassium dichromate, however, only sodium selenate reduced its effect, whereas sodium selenite and selenous acid exacerbated DNA damage. In laboratory 2 (Spain), in the TK6 lymphoblastoid cell line, the Comet assay showed that sodium selenite was non-genotoxic, while potassium dichromate and hydrogen peroxide induced DNA damage. It was also shown that sodium selenite did not decrease the genotoxicity of potassium dichromate or hydrogen peroxide when administered as a pre-treatment or at the same time, or when potassium dichromate and sodium selenite treatments were for different time periods. Thus, only sodium selenate has shown antigenotoxic properties against potassium dichromate in the Ames test and in human lymphocytes in the Comet assay.

Comet Assay↗
PubMed1990

Synthesis and antihypertensive activity of 4-(1,2-dihydro-2-oxo-1-pyridyl)-2H-1-benzopyrans and related compounds, new potassium channel activators.

The synthesis and antihypertensive activity of 4-(1,2-dihydro-2-oxo-1-pyridyl)-2H-1-benzopyran-3-ols are described. The unsubstituted pyridone adduct lead compound 7e is highly active, with substituents on the pyridone ring leading to a decrease in activity. Strongly electron-withdrawing substituents at the C-6 position are required for optimal activity. When the 2-pyridone ring is replaced by other heterocycles such as 4-pyridone, pyrimidone, pyridazinone, pyrazinone, and 1,4-butanesultam, the activity is maintained. The removal of the 3-hydroxy function (----17a) does not significantly reduce the activity. The elimination of water from the chromanols leads to the formation of the chromenes, which are among the most potent antihypertensives known. The influence of diverse substituents, in particular heterocyclic C-6 substituents, was investigated in the 4-(2-oxo-1-pyrrolidinyl)chroman-3-ol series. Chromanols esterified at the 3-hydroxy group with short-chain acids, maintain their activity. The epoxidation of the chromene double bond also produces active compounds. The rearrangement of the epoxides 22 produces the 3-keto compounds 23 and the enol derivatives 25. The reduction of the ketone 23a produces cis-chromanol 7ab along with its trans isomer 7e. All compounds were tested for oral antihypertensive activity in spontaneously hypertensive rats with a dose of 1 mg/kg; for selected compounds ED30 values as well as the duration of the antihypertensive effect were determined. 4-(1,2-Dihydro-2-oxo-1-pyridyl)-2,2-dimethyl-2H-1-benzopyran-6- carbonitrile (18a) is under development as a coronary vasodilator and a drug for treating angina pectoris.

Animals↗
PubMed1993

Interactions of guanidine and a related compound with potassium channels in frog myelinated nerve fibre.

The effects of guanidine and dimethyl guanidine were studied on current- and voltage-clamped nodes of Ranvier, to determine the electrophysiological basis for the guanidine-induced increase in neurotransmitter release. When added to the external solution, guanidine produced positive shifts of K and Na conductance-voltage curves. As a consequence, we observed a decrease of ionic flux through K channels, as well as through Na channels, and the resultant prolongation of the action potential. In addition, guanidine slowed down the time course of K current activation and reduced the percentage of inactivated Na channels. The main effect of guanidine is thus to induce depolarizing shifts of the potential dependence of K and Na channel gating parameters. Guanidine, like divalent cations, may alter the density of fixed negative charges on the outside membrane surface. The results of the action of dimethyl guanidine imply that, in addition to possible unspecific screening of the negative surface charges by cations, some specific interactions are involved. In conclusion, the prolongation of the action potential attributable to the effect of guanidine on external surface charges might contribute to the action of the drug in facilitating transmitter release by allowing the entry of more Ca ions into nerve endings.

Animals↗