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ketone/царевица

Линкът е запазен в клипборда
СтатииКлинични изследванияПатенти
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Purification and characterization of benzoyl-L-arginine p-nitroanilide hydrolase from etiolated leaves of Zea mays.

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Benzoyl-L-arginine p-nitroanilide hydrolase in the etiolated leaves of Zea mays L. has been purified 1,266-fold by a combination of gel filtration, ion exchange, and hydrophobic chromatography with a recovery of 13%. The specific activity of the purified enzyme is 5.7 units/mg protein. The enzyme is

Ketone potentiation of haloalkane-induced hepatotoxicity: CCl4 and ketone treatment on hepatic membrane integrity.

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Previous results in male Sprague-Dawley rats indicate that acetone (A), methyl ethyl ketone (MEK), and methyl isobutyl ketone (MiBK) pretreatments (3 d, p.o.) at a dosage of 6.8 mmol/kg potentiate CCl4 hepatotoxicity. The potentiation potency profile observed was MiBK > A > MEK. In the present

Vitamin E protects against methyl ethyl ketone peroxide-induced peroxidative damage to rat brain DNA.

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Peroxidative damage to DNA initiated by methyl ethyl ketone peroxide, a potent initiator of lipid peroxidation, and protection against this damage by vitamin E were studied in rats. Groups of rats were fed a casein-based diet that contained 10% tocopherol-stripped corn oil and either 0, 3, 5, or 10

Pharmacological and metabolic interactions between ethanol and methyl n-butyl ketone, methyl isobutyl ketone, methyl ethyl ketone, or acetone in mice.

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Methyl n-butyl ketone (MnBK), methyl isobutyl ketone (MIBK), methyl ethyl ketone (MEK), and acetone are widely used industrial solvents to which certain groups of workers are exposed. Pharmacological and metabolic interactions between these solvents and ethanol were explored in male CD-1 mice. The

Dose-response relationships in ketone-induced potentiation of chloroform hepato- and nephrotoxicity.

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Chloroform (CHCl3)-induced hepato- and nephrotoxicity was evaluated in male, Fischer 344 rats pretreated with various dosages (1.0 to 15.0 mmol/kg, po) of acetone (Ac), 2-butanone (Bu), 2-pentanone (Pn), 2-hexanone (Hx), or 2-heptanone (Hp). The CHCl3 challenge dosage (0.5 ml/kg, ip) produced slight

Metabolites and ketone body production following methyl n-butyl ketone exposure as possible indices of MnBK potentiation of carbon tetrachloride hepatotoxicity.

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While the biotransformation of methyl n-butyl ketone (MnBK) in animals is well characterized, little is known about the quantitative relationship between hepatic and plasma MnBK concentrations. This study provides such information and emphasizes the usefulness of MnBK metabolite quantification, as

Effect of vitamin E on pentane exhaled by rats treated with methyl ethyl ketone peroxide.

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One useful method to monitor in vivo lipid peroxidation is the measurement of volatile hydrocarbons, mainly pentane and ethane, that derive from unsaturated fatty acid hydroperoxides. Vitamin E, the biological antioxidant, inhibits lipid peroxidation and the production of pentane and ethane. The

Evidence for the involvement of organelles in the mechanism of ketone-potentiated chloroform-induced hepatotoxicity.

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Ketones can potentiate the hepatotoxicity of haloalkanes in animals. This may be due, in part, to changes in organelle susceptibility. Male Sprague-Dawley rats were administered 15 mmol/kg (po) acetone, 2-butanone, 2-hexanone or 50 mg/kg (po) chlordecone or mirex (a nonketonic analog of

Modulation of hexachlorobenzene-induced hepatic porphyria by methyl isobutyl ketone in the rat.

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Potential toxic interaction between hexachlorobenzene (HCB) and methyl isobutyl ketone (MiBK) was investigated using two different schedules of toxicant administration. The first schedule involved simultaneous administration of HCB (50 mg/kg/d, p.o. in 10 ml/kg corn oil at 10.00 a.m. for 5 d/wk) and

Tissue concentrations of methyl isobutyl ketone, methyl n-butyl ketone and their metabolites after oral or inhalation exposure.

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Quantitative relationships between plasma, liver and lung methyl isobutyl ketone (MiBK) and methyl n-butyl ketone (MnBK) concentrations after oral or inhalation exposure were established. Their respective metabolites (4-methyl-2-pentanol, 4-hydroxy-methyl isobutyl ketone, 2-hexanol, and

An in vivo mouse micronucleus assay on musk ketone.

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Musk ketone (3,5-dinitro-2,6-dimethyl-4-tert-butyl-acetophenone) was evaluated in an in vivo mouse micronucleus assay. Male and female mice were dosed with 250, 500 or 1000 mg musk ketone/kg body weight by a single intraperitoneal injection in corn oil. Results of the assay showed that under the

Effects of dietary oils and methyl ethyl ketone peroxide on in vivo lipid peroxidation and antioxidants in rat heart and liver.

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Weanling male Sprague-Dawley rats were fed diets for four weeks which differed in their content of n-6 (corn oil; CO) and n-3 fatty acids (fish oil; FO), but were similar in their content of saturated and monounsaturated fatty acids and vitamin E. At the end of the four-week feeding period, each

Long and medium chain triglycerides increase plasma concentrations of ketone bodies in suckling rats.

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The potential of medium chain triglyceride (MCT) and long chain triglyceride (LCT) as sources of plasma ketones was investigated in suckling rats. Initially high concentrations of plasma ketones in 6-, 10, and 17-day-old rats increased 2- to 3-fold after acute feeding of MCT. This feeding had the

Pharmacodynamic and metabolic interactions between ethanol and two industrial solvents (methyl n-butyl ketone and methyl isobutyl ketone) and their principal metabolites in mice.

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MnBK and MiBK prolong the duration of ketamine-, pentobarbital-, thiopental- and ethanol-induced loss of righting reflex (LRR) in mice. In equimolar doses, (5 mmol/kg i.p.), both isomers were equipotent with respect to the enhancement of ketamine-, pentobarbital-, and thiopental-induced LRR.

The effects of 5-bromo-2-thienyl-ethyl-ketone thiosenicarbazone on ovarian cyclicity and ovulation in the rat.

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Pseudopregnant and cyclic rats were injected for 5 to 26 days with daily doses of 5 and/or 3 mg of 5-bromo-2-thienyl-ethyl-ketone thiosemicarbazone (70026) starting on Day 0 (the day of oestrus). The vaginal smear cytology, record of ovulation and ability to breed and conceive were compared with the
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