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Biomedical subjects

J A Castro

Publications and source records attributed to J A Castro.

At least 199 records · Page 11Linked to original sources
PubMed1978

Carbon tetrachloride activation, lipid peroxidation and liver necrosis in different strains of mice.

Males from three different strains of mice (GXF; CF1, and Swiss) were compared in their liver response to CCl4 effects. They were capable to intensively activate CCl4 to .CCl3. No CCl4 induced lipid peroxidation was detected in the liver microsomes from any of them. All the strains remakably responded to the CCl4 induced liver damage. Results further strengthen our previous hypothesis that covalent binding of CCl4 reactive metabolites to cellular constituents is more important in relation to liver cell injury than early changes in lipid peroxidation.

Animals↗
PubMed1978

In vitro and in vivo effects of promethazine (Phenergan) on drug metabolism.

Prolongation effects of promethazine on the pentobarbital sleeping time are not due to interactions of this drug with cytochrome P-450 or cytochrome c reductase or inhibition of drug metabolism because pentobarbital plasma levels in promethazine treated animals before awakening are not different than in controls. Results suggest additive effects of both drugs on the central nervous system. Those interactions do however play a role during in vitro studies.

Animals↗
PubMed1977

Spectral changes resulting from the interaction of some N-alkyl nitrosamines and rat liver microsomes.

Dimethyl (DMN) and diethyl nitrosamine (DEN) do not give characteristic spectral changes upon interaction with rat liver microsomes, while dipropyl (DPN) and dibutyl (DBN) nitrosamine cause type I spectral changes. The spectral binding constant is 100 mM for DPN and 1.17 mM for DBN. The maximal spectral change is 3.2 X 10(6) and 1.0 X 10(6) absorbance units per milligram protein for DPN and DBN respectively.

Animals↗
PubMed1976

Further studies on the mechanism of the carbon tetrachloride induced polysome breakdown.

CCl4 ability to cause polysome breakdown in liver is age-dependent being negligible in the 7 days old rat and abruptly changing to adult values after 14 days of age. The CCl4 induced polysome breakdown process is more intense in the phenobarbital treated than in control rats while the 3-MC prior treatment does not modify its intensity. Prior treatment with SKF 525A increases the intensity of the polysome breakdown process while Sch 5705 or Sch 5706 administration do not modify it. Aminotriazole or cycloheximide pretreatment but not pyrazole administration decrease the intensity of polysome rupture caused by CCl4. The CCl4 deleterious action on strain A/J mouse liver polysomes is as intense as is in the rat liver. Results are discussed in relation to the role of either the irreversible binding of CCl4 components to ribosomes or lipid peroxidation as reponsible for the breakdown process.

Age Factors↗
PubMed1976

Toxicity of methyl bromide and other gaseous insecticides to Triatoma infestans.

Cuticular penetration of lipid soluble substances in Triatoma infestans is very poor (less than 1% in 24 hr), while the respiratory route is particularly efficient (28% in 5 min). Accordingly, several noxious gases killed the insect at short periods of time. CH3Br and SO2 were particularly effective and they also evidenced ovicide action. With the former compound this effect is also observed at low concentrations. The CH3Br hydrolysis products or its metabolites were not similarly effective, while other methylating agent, diazomethane, was very active. The irreversible binding of 14CH3Br to proteins and lipids of T. infestans, as well as the decrease in the sulfhydryl groups content of the proteins of the insect provoked by CH3Br suggest that this compound kills the insect because of its alkylating properties. The use of gaseous insecticides in the chemical control of T. infestans is discussed.

Animals↗
PubMed1976

CC14 administration to strain A/J mice or rats and the arachidonic acid content of their liver microsomal prospholipids.

CC14 administration of Sprague-Dawley male rats causes a significant decrease in the arachidonic acid content of their liver microsomal phospholipids. On the contrary, its administration to strain A/J male mice does not modify the concentration during periods of intoxication up to 24 hr. Since this strain of mice is more susceptible to CC14-induced injury than the rat, results indicate that lipid peroxidation can not be the key event in damage induced by this haloalkane.

Animals↗
PubMed1975

Irreversible binding of carbon tetrachloride to microsomal phospholipids. Free radical nature of the reactive specie and alterations in the physico-chemical properties of the target fatty acids.

Thin layer and gas liquid chromatographic analysis of the fatty acid methyl esters derived from liver microsomal phosphatidylcholine from animals treated with 14CC1-4 revealed a very similar composition to that observed during the analysis of the reaction products arised by the in vitro benzoyl peroxide initiated CC1-4 chemical addition to double bonds of fatty acid methyl esters or to fatty acids in phospholipids later transformed to methyl esters. The well known CC1-3 free radical nature of this in vitro chemical reaction gives support to the possibility for a CC1-3 free radical formation in vivo.

Animals↗
PubMed1975

Carbon tetrachloride induced polysome breakdown. Relative importance of lipid peroxidation and of binding to ribosomal components in the process.

In vivo, CC1-4 causes an intense polysome breakdown; CHC1-3 effect is much less intense and CH2C1-2 effect is negligible. Previous administration of either diphenyl-p-phenyelnediamine or alpha-tocopherol to the rats does not prevent CC1-4-induced polysome breakdown. Promethazine and cystamine were able to prevent to a good extent the CC1-4 induced polysome breakdown process. 14CC1-4 irreversibly binds to ribosomal proteins but not to ribosomal RNA. Several hepatocarcinogens which are effective alkylating agents and cause in vivo polysome breakdown do not induce a lipid peroxidation process.

Animals↗