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M Orellana

Publications and source records attributed to M Orellana.

At least 19 recordsLinked to original sources
PubMed1998

Effects of chronic ethanol consumption on extramitochondrial fatty acid oxidation and ethanol metabolism by rat kidney.

1. We evaluated the effects of chronic ethanol consumption on microsomal and peroxisomal fatty acid oxidation and on ethanol oxidation by the kidney. 2. When mature rats were fed 20% ethanol for 10 weeks, an increase in alcohol dehydrogenase and catalase activities were observed in the kidney. 3. Renal microsomal and peroxisomal oxidation of fatty acids also increased by the treatment, but total cytochrome P450 content did not. 4. We concluded that chronic ethanol consumption results in an increased extramitochondrial disposition of fatty acids and ethanol oxidation by the kidney.

Alcohol Dehydrogenase↗
PubMed1998

Acute and chronic effect of ethanol on (Na + K)-ATPase activity and cyclic AMP response to vasopressin in rat papillary collecting duct cells.

1. We evaluated the effects of ethanol on (Na + K)-ATPase activity and cAMP response to vasopressin in native and cultured rat papillary collecting duct (PCD) cells. 2. A significant increase in (Na + K)-ATPase and Mg(2+)-ATPase activities was found in PCD cells either isolated from chronic ethanol-fed rats or cultured in the presence of ethanol. 3. Acute treatment with ethanol resulted in a biphasic effect on the activity of (Na + K)-ATPase, which was enhanced below 1% ethanol and inhibited at higher concentrations. 4. Chronic ethanol treatment did not change the cAMP response of PCD cells to vasopressin. Acutely, in turn, this response was enhanced by ethanol per se. 5. It is suggested that the antinatriuretic effect of ethanol could be at least in part mediated by a (Na + K)-ATPase enhancement in PCD cells. Acutely, ethanol could normalize water balance by its peripheral effects on distal nephron.

Animals↗
PubMed1997

Microsomal and peroxisomal fatty acid oxidation in streptozotocin diabetic rat liver.

Microsomal lauric acid hydroxylation and fatty acid peroxisomal beta-oxidation were studied in hepatic subcellulant preparations from streptozotocin-induced diabetic and diabetic insulin-treated rats. 2. The liver microsomes of the streptozotocin diabetic rats displayed a similar activity to hydroxylate lauric acid as the control microsomes. 3. Diabetic insulin-treated rats showed lower (omega 1) and omega-lauric acid hydroxylase activities than diabetic and control rats. 4. Streptozotocin-induced diabetes and diabetic insulin-treated rats exhibited no significant changes on peroxisomal palmitoyl CoA beta-oxidation compared to the control rats. 5. Both microsomal and peroxisomal fatty acid oxidation responded in a similar way in this model of experimental diabetes.

Animals↗
PubMed1997

Microsomal and peroxisomal fatty acid oxidation in bile duct ligated rats: a comparative study between liver and kidney.

1. Microsomal cytochrome P-450 and peroxisomal fatty acid oxidation was studied in the kidney of rats 7 days after bile duct ligation (BDL) and a comparative study between kidney and liver was done. 2. Only in the liver did cholestasis decrease the cytocrome P-450 content and the peroxisomal fatty acid beta-oxidation, the catalase activity, and the microsomal metabolism of lauric acid and aminopyrine. 3. In contrast, cholestasis did not influence these activities in the kidney. The microsomal and peroxisomal activities studied responded in a coordinate way to cholestasis. 4. These results could suggest the possibility of a cause-and-effect relationship between microsomal cytochrome P-450 and peroxisomal activity.

Aminopyrine↗
PubMed1997

Microsomal and peroxisomal fatty acid oxidation in liver of rats with bile duct ligation and two-thirds hepatectomy.

Microsomal cytochrome P450 and peroxisomal activity were studied in liver of rats 7 days after two-thirds hepatectomy or bile duct ligation (BDL). Both surgical models decreased the hepatic microsomal cytochrome P450 content, but only cholestasis, produced by BDL, decrease the microsomal metabolism of lauric acid and aminopyrine, peroxisomal fatty acid beta-oxidation and catalase activity. The microsomal and peroxisomal activities responded in a coordinate way to cholestasis and two-thirds hepatectomy. These results suggest a cause-effect relationship between the microsomal cytochrome P450 and peroxisomal activity.

Animals↗
PubMed1995

Dietary fish oil and cytochrome P-450 monooxygenase activity in rat liver and kidney.

Lauric acid hydroxylation and aminopyrine N-demethylation were studied in kidney and liver microsomes from rats treated with fish oil. Different doses of fish oil containing 20% eicosapentaenoic acid and 10% docosahexaenoic acid were provided daily to the rats for seven days. In all the groups studied, the lauric acid metabolism was higher in kidney microsomes and the aminopyrine metabolism in the liver microsomes. Although no effect on the renal cytochrome P-450 concentration was detectable, all four fish oil doses increased the hepatic concentration of cytochrome P-450 by a mean 27%. The higher fish oil doses used increased the renal and hepatic microsomal metabolism of aminopyrine. The lauric acid metabolism was increased by fish oil only in the liver. Fish oil, a known inducer of fatty acid peroxisomal beta-oxidation, also induced microsomal activity. These results show that liver and kidney respond in different ways to dietary factors such as fish oil. In addition, our study would suggest that fish oil increased the activity of two different families of liver cytochrome P-450. The activity of kidney lauric acid 11- and 12-hydroxylation, however, was not modulated by fish oil.

Aminopyrine↗
PubMed1993

Starvation effect on rat kidney peroxisomal and microsomal fatty acid oxidation. A comparative study between liver and kidney.

Microsomal lauric acid 12-hydroxy lauric acid (omega)-hydroxylation and fatty acid peroxisomal beta-oxidation were studied in kidney tissue from starved rats. Starvation increased the microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids with a high correlation between both processes. Earlier, we reported similar results in liver. Our results support the hypothesis that the role of microsomal fatty acids omega-hydroxylation is the generation of substrate for peroxisomal beta-oxidation, with the final purpose of contributing to a catabolic or gluconeogenic pathway from fatty acids.

Animals↗
PubMed1992

Modulation of rat liver peroxisomal and microsomal fatty acid oxidation by starvation.

In this work the microsomal lauric acid omega-hydroxylation, fatty acid peroxisomal beta-oxidation, and the levels of cytochrome P-450 IVA1 were studied in liver tissue from starved rats. Starvation increased the peroxisomal beta-oxidation and the microsomal hydroxylation of fatty acids. The correlation between these activities would support the proposal that both processes are linked, contributing in part to catabolism of fatty acids in liver of starved rats.

Animals↗
PubMed1991

Treatment of acute toxoplasmosis with intravenous clindamycin. The California Collaborative Treatment Group.

The interim results are presented of an ongoing large-scale, prospective, randomized study to determine the potential role of clindamycin in the treatment of toxoplasmic encephalitis. Patients were seropositive for Toxoplasma gondii antibodies and had clinical signs compatible with toxoplasmic encephalitis. Data was available on 33 patients, 15 of whom received pyrimethamine p.o./clindamycin i.v. and then p.o., and 18 of whom received pyrimethamine p.o./sulfadiazine p.o. The interim evaluation did not reveal a remarkable difference between the two regimens in the clinical or radiologic response. Adverse reactions to both regimens were common and frequently multiple, there being more adverse gastrointestinal reactions in patients on pyrimethamine/clindamycin and more adverse hematological reactions in those on pyrimethamine/sulfadiazine.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Nutritionally triggered alterations in the regiospecificity of arachidonic acid oxygenation by rat liver microsomal cytochrome P450.

Cytochrome P450-dependent oxidation of arachidonic acid was studied in liver microsomes from normal fed, protein-energy malnourished, and refed rats. The overall rate of arachidonic acid oxidation was very similar in microsomes from the three groups, but microsomes from malnourished rats showed a higher turnover rate than microsomes from normal fed and refed rats. The regiospecificity of cytochrome P450 oxidation of arachidonic acid was drastically altered by the animal nutritional status. Thus, protein-energy malnutrition results in a clear stimulation of total omega and omega-1 hydroxylation, concomitant with a marked decrease in olefin epoxidation and allyllic oxidations. These changes, as well as the documented biological activity of some of the cytochrome P450 arachidonate metabolites, suggest that protein-energy deficiency might help to select P450 isozymes which are probably involved in key monooxygenation reactions of physiological substrates.

Animals↗
PubMed1988

Purification and characterization of liver cytochrome P-446 isolated from protein energy malnourished rats.

A liver cytochrome P-450 isozyme has been purified to homogeneity from protein-energy malnourished rats induced with beta-naphthoflavone (beta-NF). The purification steps included chromatography on DEAE-Sephadex-A-25, DEAE-cellulose (DE-53), hydroxylapatite (HA) and carboxymethyl-sephadex (CM) columns. The reduced carbon monoxide difference and absolute spectra showed a Soret peak at 446.5 nm. The wavelength maxima for the oxidized and reduced spectra were at 416 and 408 nm, respectively. Cytochrome P-446 appears to have a predominantly low spin ferric iron, migrates as a single band of molecular weight 56,000 in sodium dodecyl sulfate polyacrylamide gels and has a specific content of 14 nmol/mg of protein. P-446 oxidized various substrates at different rates in a reconstituted system with NADPH-cytochrome P-450 reductase and dilauroyl-phosphatidylcholine. In this system turnover rates for benzo[alpha]pyrene, testosterone and benzphetamine oxidation were: 81.10; 1.85 and 1.42 nmoles product/min/nmol P-446 respectively. While NH2 terminal amino acid sequence analysis of 18 of the first 20 residues suggests that the cytochrome P-446 isolated from malnourished rats is identical with form c, the catalytic activities suggest that this isozyme may be a more effective or efficient catalyst for some substrates.

Animals↗
PubMed1988

Inhibitors of cytochrome P-450-dependent arachidonic acid metabolism.

A new generation of heteroatom analogs of arachidonic acid are documented as powerful and selective inhibitors of the cytochrome P-450-dependent arachidonic acid oxygenase reaction (IC50, 5-10 microM) with little effect on either cyclooxygenase or soybean lipoxidase at 100 microM. The imidazole derivatives, ketoconazole and clotrimazole, are potent and selective inhibitors of the arachidonic acid epoxygenase and lipoxidase-like activities of phenobarbital-induced rat liver microsomal fractions (IC50, 2.0 and 0.3 microM, respectively). In contrast, the w/w-1 oxygenase activity of ciprofibrate-induced microsomal fractions was relatively resistant to inhibition by these compounds (IC50, 50 and 25 microM for ketoconazole and clotrimazole, respectively). Nordihydroguaiaretic acid (NDGA), eicosatetraynoic acid (ETYA), and indomethacin, extensively utilized inhibitors of the cyclooxygenase and lipoxygenase branches of the arachidonate cascade, also inhibit cytochrome P-450-dependent arachidonic acid metabolism. In decreasing order of potency, they were NDGA, ETYA, and indomethacin (IC50, 15, 40, and 70 microM, respectively).

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1988

Nutrition-related alterations in liver microsomal testosterone hydroxylases.

The oxidation products of testosterone formed by liver microsomes from normal-fed and protein-energy malnourished male rats have been analysed by HPLC. Microsomes from normal-fed rats oxidized testosterone at a rate of 4.52 nmol/min/mg protein. The major products formed were: 6 beta-, 7 alpha- and 16-alpha-hydroxytestosterone; these three metabolites represented 65% of the total testosterone metabolism. Microsomes from protein-energy malnourished rats oxidized testosterone at a reduced rate of 2.03 nmol/min/mg protein. The major product formed was 7 alpha-hydroxytestosterone, which accounted for 43% of total testosterone oxidation. Microsomes from protein-energy malnourished rats showed a CO-reduced cytochrome P-450 spectra with a maxima at 452 nm, and a 38% decrease in the total content of cytochrome P-450. Some testosterone hydroxylases were drastically affected by protein-energy malnutrition but others, such as 7 alpha-hydroxylase, remained unchanged. The present results suggest that nutritional status can modify the relative amounts of individual cytochrome P-450 isozymes, thus explaining the observed changes in several testosterone hydroxylases. Protein-energy malnutrition seems to be an excellent tool with which to obtain a microsomal fraction containing predominantly P-450 isozymes, which are probably involved in key mono-oxygenations of physiological substrates.

Animal Nutritional Physiological Phenomena↗
PubMed1981

Epidemiology of gastric cancer in Chile: I - Case-control study.

The results of a case-control study of stomach cancer carried out with the collaboration of 7 participating hospitals in Santiago, Chile are reported. Patients attending gastroscopy clinics were interviewed before or after gastroscopy. The diagnosis was unknown to either the patient or the interviewer at the time of interview. 360 stomach cancer cases were subsequently matched to non-cancer patients selected from the pool interviewed at the same time as the cases. Study findings show: 1) longer-term residence in high-risk areas in early life by cases than controls; 2) an association between stomach cancer and a prior occupation in agriculture. In a subgroup of 98 cases for whom histologic classification was available, the association with residence in early life in a high-risk area was seen only for cases with intestinal-type stomach cancer.

Adult↗
PubMed1981

Epidemiology of gastric cancer in Chile: II - Nitrate exposures and stomach cancer frequency.

Nitrate levels in urine and nitrite levels in saliva were determined in school children 11-13 years of age in 2 areas of high stomach cancer mortality located in central Chile and in 2 areas of low stomach cancer mortality located at the extremes of Chile. Levels of both nitrates and nitrites were concurrently determined in selected vegetables obtained in these 4 study areas. Levels of nitrates were significantly higher in the urine of schoolchildren and in vegetables obtained from the northern low-risk area. Levels of nitrites were similar in saliva specimens from all 4 areas, but levels in vegetables were inconsistent. These results are apparently incompatible with the hypothesis of a high nitrate intake in areas of high stomach cancer incidence compared to areas of low incidence. This paradoxical finding suggests that cofactors may be involved in the pathopoiesis of stomach cancer that promote or inhibit the transformation of dietary nitrates to nitrosamines. The soil in the high-risk areas is primarily of volcanic origin, which is reported to be low in levels of selenium. On the other hand, residents of Antofagasta, the northern low-risk area, are known to be exposed to high levels of arsenic. It is possible that the diet of residents of the high incidence area which may be deficient in selenium may enhance promotion of nitrates to nitrosamines as has been reported in the literature, or conversely, that high levels of arsenic or other factors in the diet of individuals in Antofagasta may play a protective role. Other factors may be responsible for the low rate observed in the southern low-risk area.

Adolescent↗