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At least 19 recordsLinked to original sources
PubMed1992

A simple enzymatic quantitative analysis of triglycerides in tissues.

We determined a method to measure the triglyceride levels in tissues by using a modified enzymatic kit. This enzymatic kit was originally designed to be used to measure the triglyceride levels in plasma. Our method of triglyceride level determination includes dissolving the tissue lipid extracts in an alcohol. Before using the enzymatic kit directly, the lipids were dissolved in tert-butyl alcohol, then a Triton X-100/methyl alcohol mixture was added (1/1 by volume). The presence of organic surfactants such as tert-butyl alcohol and methyl alcohol, and of a surfactant such as Triton X-100, did not interfere with the enzymatic activity. This method enabled us to determine triglyceride levels between 10 and 90 nmol, by using a spectrophotometer to measure the absorbances.

Animals↗
PubMed1975

New synthesis of (RS)-carnitine chloride.

A four-step synthesis of (RS)-carnitine chloride was developed using extremely mild reaction conditions and versatile intermediates. Crotyl chloride was converted to tert-butyl 3-butenoate using tert-butyl alcohol and triethylamine in ether. Treatment of tert-butyl 3-butenoate with m-chloroperbenzoic acid in chloroform afforded tert-butyl 3,4-epoxybutyrate. Reaction of this compound with trimethylamine hydrochloride in methanol, followed by mild acid hydrolysis of the tert-butyl ester, afforded (RS)-carnitine chloride.

Carnitine↗
PubMed1979

Acute toxicology of butyl nitrites and butyl alcohols.

Commercially available isobutyl nitrite (iBN), n-butyl nitrite (nBN), sec-butyl nitrite (sBN) and tert-butyl nitrite (tBN) were found to be 63%, 79%, 44% and 96% pure, respectively, by GLC analysis. Pure samples of each compound were synthesized by the action of nitrous acid on each of the corresponding butyl alcohols; GLC analysis indicated greater than 99% purity for each nitrite. In determining LD50 values (mice, i.p.) for each compound, no deaths were observed after 30 min post-administration of sBN or tBN. Gross post-mortem examination suggests the delayed lethality may be due to liver damage. Administration of isobutyl, n-butyl, sec-butyl or tert-butyl alcohols to mice produced similar hepatotoxicity, suggesting that butyl alcohols may play a role in the hepatotoxicity observed after sBN or tBN administration.

Animals↗
PubMed1979

Progestin permeation through polymer membranes III: Polymerization solvent effect on progesterone permeation through hydrogel membranes.

Hydrogels prepared from poly(hydroxyethyl methacrylate) are biocompatible and highly permeable to low molecular weight solutes. Permeation rates can be varied by altering the cross-linker concentration or using copolymers; the latter are chosen to alter the hydrogel equilibrium hydration. These factors suggest that hydrogels are good candidates for controlled-release drug delivery devices. Hydrogels may be synthesized using various temperatures, initiators (nature and concentration), and solvents (nature and concentration). This study demonstrated that progesterone permeation through poly(hydroxyethyl methacrylate) films is independent of polymerization solvent (nature and concentration) for the solvents, water, ethanol, and tert-butyl alcohol. The importance of hydrogel equilibrium hydration in progesterone permeation is emphasized.

Acrylic Resins↗
PubMedDate not supplied

DNA damage induced by metabolites of o-phenylphenol in the presence of copper(II) ion.

Reactivities of o-phenylphenol and its metabolites (2,5-dihydroxybiphenyl, 2-phenyl-1,4-benzoquinone) with DNA were investigated by a DNA sequencing technique, and the reaction mechanism was studied by UV-visible and ESR spectroscopies. In the presence of Cu(II), 2,5-dihydroxybiphenyl caused strong DNA damage even without piperidine treatment. Catalase, methionine, and methional inhibited the DNA damage completely, whereas mannitol, sodium formate, ethanol, tert-butyl alcohol, and superoxide dismutase did not. 2,5-Dihydroxybiphenyl plus Cu(II) frequently induced a piperidine-labile site at thymine and guanine residues. The addition of Fe(III), Mn(II), Co(II), Ni(II), Zn(II), Cd(II), or Pb(II) did not induce DNA damage with 2,5-dihydroxybiphenyl. When H2O2 was added, 2-phenyl-1,4-benzoquinone also induced DNA damage in the presence of Cu(II). Cu(II) accelerated the autoxidation of 2,5-dihydroxybiphenyl to quinone. An ESR study revealed that the semiquinone radical is an intermediate of the autoxidation. Catalase had no inhibitory effect on the acceleration by Cu(II). Superoxide dismutase promoted both the autoxidation of 2,5-dihydroxybiphenyl and the initial rate of semiquinone radical production. ESR spin trapping experiments showed that the addition of Fe(III) produced hydroxyl radical during the autoxidation of 2,5-dihydroxybiphenyl, whereas the addition of Cu(II) hardly did so. The results suggest that DNA damage by 2,5-dihydroxybiphenyl plus Cu(II) is due to active species other than hydroxyl free radical.

Benzoquinones↗
PubMed1991

Alcohols protect Escherichia coli against cold shock.

Alcohols protect Escherichia coli against cold shock, and the concentration of alcohol which provided optimal protection declined with increasing hydrophobicity of the alcohol. The rate of loss of viability after the chilling transition was decreased by n-octanol, even when it was added after that chilling transition. Cold-shocked cells exhibited a sensitivity toward dioxygen, seen as greater enumeration on anaerobic, rather than on aerobic, trypticase-yeast extract agar plates, and addition of catalase or antioxidants, such as alpha-tocopherol or probucol, to the agar plates did not lessen this dioxygen sensitivity. Respiratory capacity was diminished by cold shock, and cyanide-sensitive respiration was more affected than was cyanide-resistant respiration. Discharging the proton gradient, with the uncoupler carbonyl cyanide trifluoromethoxy-phenylhydrazone, did not change sensitivity to cold shock. There was no evidence for minimal medium recovery after cold shock. The data presented, as well as that already in the literature, are explained on the basis of membrane damage caused by patches of ordering transitions in one membrane leaflet, unmatched by comparable transitions in the mating leaflet.

1-Octanol↗
PubMed1991

Ethanol oxidation is not required to attenuate endotoxin-enhanced glucose metabolism.

Previous studies from our laboratory demonstrated that acute ethanol (EtOH) intoxication, through an unknown mechanism, blunts the endotoxin-enhanced carbohydrate metabolism. The purpose of the present study was to determine whether oxidation of the ethanol moiety is required for the inhibition of the endotoxin-induced changes in carbohydrate metabolism. In vivo glucose kinetics were assessed by the intravenous administration of D-[3-3H]glucose in catheterized conscious unrestrained rats. Escherichia coli endotoxin (200 micrograms/100 g body wt) increased glucose rate of appearance (Ra) and metabolic clearance rate (MCR) by 75 and 50%, respectively. A primed-constant infusion of EtOH (275 mg/100 g + 25 mg.100 g-1.h-1) initiated 2 h before endotoxin challenge attenuated the endotoxin-enhanced glucose kinetics. EtOH intoxication did not prevent endotoxin-induced hyperglycemia but delayed the hyperlactacidemic response. The importance of EtOH metabolism in suppressing the glucose metabolic response to endotoxin was studied by administering 4-methyl-pyrazole (4-MP; 8 mg/100 g), an inhibitor of alcohol dehydrogenase activity. After administration of 4-MP and a bolus injection of EtOH (275 mg/100 g), the plasma EtOH concentration remained constant and matched the level of EtOH in rats receiving a primed-constant infusion of EtOH. Inhibition of EtOH metabolism with 4-MP did not abrogate the ability of EtOH to suppress endotoxin-induced increases in glucose Ra or MCR. Furthermore, the injection of the nonmetabolized alcohol tert-butanol abolished the endotoxin-induced increase in glucose Ra and MCR without preventing the endotoxin-induced hyperglycemia and hyperlactacidemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Dehydrogenase↗
PubMed1992

Subchronic toxicity studies of t-butyl alcohol in rats and mice.

The purpose of this study was to evaluate the toxicity of t-butyl alcohol, an important commodity chemical, an additive to unleaded gasoline, and a contaminant of drinking water. Ninety-day toxicity studies were conducted in B6C3F1 mice and Fischer 344 (F344) rats of both sexes using dosed water. Dose levels of t-butyl alcohol were 0, 0.25, 0.5, 1, 2, and 4% (w/v). Lethality was observed at the 4% level of both sexes and species. Weight-gain depression was present in all dose levels of male rats; 4% female rats; 1, 2, and 4% male mice; and 2 and 4% female mice. Water consumption was increased at lower dose levels in male rats and decreased in the higher dose levels of both sexes of rats and female mice. Clinical signs in rats were ataxia in both sexes and hypoactivity in males. Clinical signs in mice were ataxia, abnormal posture, and hypoactivity. In rats, urine volumes were reduced, in association with crystalluria. Gross lesions at necropsy were urinary tract calculi, renal pelvic and ureteral dilatation, and thickening of the urinary bladder mucosa. Microscopic lesions were hyperplasia of transitional epithelia and inflammation of the urinary bladder. In male rats treated with t-butyl alcohol, microscopic renal changes were suggestive of alpha-2 mu-globulin nephropathy. No-effect levels for the urinary tract lesions were 1% in male rats and mice (803.7 mg/kg/day for the male rats and 1565.8 mg/kg/day for the male mice) and 2% in female rats and mice (1451.5 mg/kg/day for the female rats and 4362.9 mg/kg/day for the female mice). The results indicate that in rodents the urinary tract is the target organ for t-butyl alcohol toxicity, and males are more sensitive to t-butyl alcohol toxicity than females.

Animals↗
PubMed1991

Can .OH scavengers protect against direct UV-C damage in vivo?

It has previously been shown that ethanol and tert-butanol protect poly(U) against strand breaks from pulsed laser ultraviolet (UV) photons (lambda = 248 nm). This protection is believed to be based on a modification of direct DNA damage, not on scavenging hydroxyl radicals. In this paper, several .OH scavengers were tested in vivo with Escherichia coli DNA repair-deficient mutants to see if protection could also be demonstrated with non-laser UV photons (lambda approximately 254 nm). No protection was observed.

Butanols↗
PubMed1990

Effects of oxygen radical scavengers on the inactivation of SS phi X174 DNA by the semi-quinone free radical of the antitumor agent etoposide.

We have studied the effects of oxygen radical scavengers on the inactivation of ss phi X174 DNA by the semi-quinone free radical of the antitumor agent etoposide (VP 16-213), which was generated from the ortho-quinone of etoposide at pH greater than or equal to 7.4. A semi-quinone free radical of etoposide is thought to play a role in the inactivation of ss phi X174 DNA by its precursors 3',4'-ortho-quinone and 3',4'-ortho-dihydroxy-derivative. The possible role of oxygen radicals formed secondary to semi-quinone formation in the inactivation of DNA by the semi-quinone free radical was investigated using the hydroxyl radical scavengers t-butanol and DMSO, the spin trap DMPO, the enzymes catalase and superoxide dismutase, the iron chelator EDTA and potassium superoxide. Hydroxyl radicals seem not important in the process of inactivation of DNA by the semi-quinone free radical, since t-butanol, DMSO, catalase and EDTA had no inhibitory effect on DNA inactivation. The spin trapping agent DMPO strongly inhibited DNA inactivation and semi-quinone formation from the ortho-quinone of etoposide at pH greater than or equal to 7.4 with the concomitant formation of a DMPO-OH adduct. This adduct probably did not arise from OH. trapping but from trapping of O2-(.). DMSO increased both the semi-quinone formation from and the DNA inactivation by the ortho-quinone of etoposide at pH greater than or equal to 7.4. Potassium superoxide also stimulated phi X174 DNA inactivation by the ortho-quinone at pH less than or equal to 7. From the present study, it is also concluded that superoxide anion radicals probably play an important role in the formation of the semi-quinone free radical from the ortho-quinone of etoposide, thus indirectly influencing DNA inactivation.

Bacteriophage phi X 174↗
PubMed1991

Acute dependence on depressant drugs is determined by common genes in mice.

Withdrawal seizure prone (WSP) and withdrawal seizure resistant (WRS) mice were genetically selected to express severe or mild handling-induced convulsions (HIC), respectively, after cessation of chronic ethanol (EtOH) vapor inhalation. The studies reported here tested WSP and WSR mice to determine whether elevated HIC were seen after administration of acute doses of several drugs that depress central nervous system activity. The drugs tested were EtOH, pentobarbital, t-butanol, acetaldehyde, and diazepam. All drugs initially suppressed HIC in WSP mice. This suppression was followed by an exacerbation of HIC, suggestive of a state of rebound central nervous system hyperexcitability during acute withdrawal. Susceptibility to acute withdrawal seizures was clearly under genetic control, since WSR mice did not display acute withdrawal HIC to any appreciable extent. Acute EtOH withdrawal seizures did not require testing WSP mice repeatedly, as they could be seen upon a single HIC test 8 hr after EtOH injection. Results with acetaldehyde and t-butanol suggest that the formation of acetaldehyde may be sufficient, but is not necessary for the elicitation of acute EtOH withdrawal. Earlier studies had found that WSP mice displayed more severe withdrawal HIC than WSR mice after chronic treatment with t-butanol, phenobarbital, nitrous oxide, or diazepam. The genetic predisposition to chronic EtOH withdrawal HIC in WSP mice generalized to all central nervous system depressants acutely tested, suggesting that acute and chronic withdrawal to all these drugs is largely under the control of a common group of genes.

Acetaldehyde↗
PubMed1990

Chronic ethanol exposure of PC 12 cells alters adenylate cyclase activity and intracellular cyclic AMP content.

Effects of chronic ethanol exposure on adenylate cyclase activity and intracellular cyclic AMP content were investigated in PC 12 cells. Stimulation of cyclic AMP content by 2-chloroadenosine (2-CADO) and forskolin were reduced after a 4-day exposure of the cells to 150 mM ethanol. Although chronic ethanol treatment did not alter 2-CADO- and NaF-stimulated adenylate cyclase activities in a cell-free preparation, 2-CADO-, forskolin, and NaF-stimulated adenylate cyclase activities were reduced when assays were carried out in saponin-treated cells. Chronic ethanol exposure also increased the ability of in vitro ethanol to stimulate adenylate cyclase activity and cyclic AMP content. The in vitro addition of tert-butanol caused a dose-dependent increase in adenylate cyclase activity, and a 4-day treatment of PC 12 cells with 50 mM tert-butanol reduced 2-CADO- and forskolin-stimulated cyclic AMP contents. Chronic treatment with tert-butanol, however, did not alter the stimulatory effects of in vitro ethanol. Similarly, a 4-day exposure to 125 mM ethanol using serum-free defined media decreased 2-CADO- and forskolin-stimulated cyclic AMP content without changing the stimulatory effects of in vitro ethanol. The increased sensitivity of adenylate cyclase to in vitro ethanol also was not observed when chronic ethanol treatment was carried out with media containing delipidated serum. The increased sensitivity to ethanol, however, was restored when the chronic ethanol treatment was carried out with serum-free defined media supplemented with serum lipoproteins.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Chloroadenosine↗
PubMed1978

Absorption and disposition of N-(1, 1-dimethylethyl)-N'-[2-(4-pyridinyl)-4-pyrimidinyl]urea in rats and dogs.

N-(1, 1-Dimethylethyl)-N'-[2-(4-pyridinyl)-4-pyrimidinyl]urea, Win 40, 882, was eliminated from the blood stream of dogs by two apparent first-order processes with alpha- and beta-phase half-lives of 0.2 hr and 1.4 hr, respectively. Radioactivity of the administered dose was excreted by rats in the feces and via the kidneys; about 40-45% of the dose was recovered in the feces, with the remainder in the urine, over a six day period. One of the terminal methyl groups of the tert-butyl moiety of Win 40,882 is sequentially oxidized by the rat to the alcohol, aldehyde and carboxylic acid. In addition, some of the aldehyde was further metabolized to generate two different monohydroxylated aldehydic metabolites; these hydroxyaldehydes accounted for less than 10% of the dose administered. An unusual metabolic pattern was noted in the excretion of Win 40,882. Over 30% of the urinary metabolites contained the carboxaldehyde function; only8% of the urinary radioactivity was represented by the further oxidation of the aldehyde group to generate the carboxylic acid.

Absorption↗
PubMed1977

[Contribution to the migration and toxicology of 2-(2'-hydroxy-3'-tert-butyl-5'-methylpheny)-5-chlorobenzotriazole].

Studies on the use of an ultraviolet-absorbing agent based on hydroxybenzotriazole for commodities of low-pressure and high-pressure polyethylene and polypropylene show that the migration is only slight in aqueous and acidic foods and in foodstuffs with low alcohol content. Sunflower oil, n-heptane (as a fat-stimulating test solution) and 50% ethanol as test solutions yielded higher migration values. Gas chromatographic, polarographic and thin-layer chromatographic methods were used to determine the ultraviolet-absorbing agent. Concerns about a possible photosensitizing effect of 2-(2'-hydroxy-3'-tert-butyl-5'-methylphenyl)-5-chlorobenzotriazole were experimentally tested and turned out to be unfounded. From the viewpoint of safety, there are no contraindications to the use of polyolefines in packing materials for most foods. As to fat-containing and strongly alcoholic foodstuffs, the authorization should be conditioned on the circumstances of use.

Animals↗
PubMed1991

Hepatoprotective and anti-inflammatory effects of a traditional medicinal plant of Chile, Peumus boldus.

Dried hydro-alcoholic extract of Peumus boldus (Monimiaceae) has been evaluated for hepatoprotective, choleretic and anti-inflammatory effects in mice and rats, in order to validate or to invalidate traditional therapeutic indications. This extract exerted a significant hepatoprotection of tert-butyl hydroperoxide-induced hepatotoxicity in isolated rat hepatocytes (in vitro technique) by reducing the lipid peroxidation and the enzymatic leakage of LDH; this in vitro efficacy was reinforced by a significant hepatoprotection on CCl4-induced hepatotoxicity in mice (in vivo technique), the plant extract reducing the enzymatic leakage of ALAT. Boldine, the main alkaloid of P. boldus appears to be implicated in this hepatoprotective activity. Choleretic effects, often mentioned in traditional indications, have not been confirmed in rats. Finally, significant and dose-dependent anti-inflammatory effects were obtained on an acute inflammatory process (carrageenan-induced edema test in rats). Boldine does not appear to be involved in such properties.

Animals↗
PubMed1992

Synthesis of racemic 5-phosphonate analogues of myo-inositol 1,4,5-tris- and 1,3,4,5-tetrakis-phosphate.

(+/-)-2,3,6-Tri-O-benzyl-5-O-p-methoxybenzyl-myo-inositol and (+/-)-2,6-di-O-benzyl-5-O-p-methoxy-benzyl-myo-inositol, accessible readily from (+/-)-3,6-di-O-allyl-1,2-O-cyclohexylidene-myo-inositol, were phosphitylated with dibenzyl N,N-di-isopropylphosphoramidite, and the resulting phosphite triesters were oxidised with tert-butyl hydroperoxide to give the corresponding fully protected myo-inositol 1,4-bis- (12) and 1,3,4-tris-phosphate (13) derivatives. Cleavage of the p-methoxybenzyl group from 12 and 13, phosphonylation with bis[6-(trifluoromethyl)benzotriazol-1-yl] methylphosphonate or (difluoromethyl)phosphonic di(1,2,4-triazolide), followed by treatment in situ with benzyl alcohol, and then hydrogenolysis of the benzyl groups gave the 5-methylphosphonate and 5-[(difluoromethyl)phosphonate] analogues of myo-inositol 1,4,5-tris- and 1,3,4,5-tetrakis-phosphate. The 5-methylphosphonate analogue of myo-inositol 1,4,5-trisphosphate acted as a calcium antagonist in permeabilized human platelets.

Blood Platelets↗
PubMedDate not supplied

Ageing of Neurospora crassa. II. Organic hydroperoxide toxicity and the protective role of antioxidant and the antioxygenic enzymes.

Cumene hydroperoxide and tert-butyl hydroperoxide at sublethal concentrations initially prevent growth of mycelia of wild-type Neurospora crassa, but after a time the cells grow at a subnormal steady-state rate. The antioxidant nordihydroguaiaretic acid protects unadapted cells from hydroperoxide inhibition, leading to a decrease in the time before growth begins, an increase in steady-state growth rate and an increase in biomass production. The results of growth transfer experiments and enzyme measurements indicated that the acquired resistance to the hydroperoxides is physiological and most likely involves the induction of the synthesis of the antioxygenic enzymes superoxide dismutase, glutathione peroxidase and glutathione reductase. Nordihydroguaiaretic acid normalizes the levels of activities of glutathione peroxidase and glutathione reductase during culture with hydroperoxide. Molecular-induced homolysis of the hydroperoxides, a process that is induced by unsaturated fatty acids of membrane lipids, leads to lipid autoxidation in a chain reaction which produces lipid hydroperoxides, which in turn decomposes to form more free radicals. Nordihydroguaiaretic acid, a well-known free radical scavenger, probably serves to minimize hydroperoxide decomposition, lipid autoxidation and molecular damage from free radicals, whereas the coupled enzyme system glutathione peroxidase and glutathione reductase minimizes these processes by decomposing the hydroperoxides to harmless alcohols. We suggest that either free radicals derived from these processes or some consequent non-radical products may serve as the inducers of this enzyme system, rather than the hydroperoxide substrates.

Aging↗