Effect of an avocado oil-rich diet over an angiotensin II-induced blood pressure response.

We studied the effect of an avocado oil-rich diet on (1) the blood pressure response to angiotensin II (AngII) and (2) the fatty acid composition of cardiac and renal membranes on male Wistar rats. The avocado oil-rich diet induced a slightly higher AngII-induced blood pressure response in the rats as compared to the control rats. In cardiac microsomes, avocado oil induced an increase in oleic acid content (13.18+/-0.33% versus 15.46+/-0.59%), while in renal microsomes, the oil decreased alpha-linolenic acid content (0.34+/-0.02% versus 0.16+/-0.12%), but increased the arachidonic acid proportion (24.02+/-0.54% versus 26.25+/-0.54%), compared to control. In conclusion, avocado oil-rich diet modifies the fatty acid content in cardiac and renal membranes in a tissue-specific manner. The rise in renal arachidonic acid suggests that diet content can be a key factor in vascular responses.

[Participation of nitric oxide and arachidonic acid metabolites via cytochrome - P450 in the regulation of arterial blood pressure]. / Participación del óxido nítrico y los metabolitos del ácido araquidónico vía citocromo P450 en la regulación de la presión arterial.

Nitric oxide and cytochrome P450 arachidonic acid metabolites participate in blood pressure regulation. The synthesis of these autacoids leads to arterial hypertension. However, it is not known whether there is an interaction between them. Therefore, we studied the modulatory effect of nitric oxide and cytochrome P450-arachidonic acid metabolites, their interaction on blood pressure, and the renal content of cytochrome P450. Male Wistar rats were divided: 1) control, 2) L-NAME (100 mg/kg/d p.o.), 3) L-NAME + SnCl2 (10 mg/kg/d i.p.), and 4) L-NAME + dexamethasone (1 mg/kg/d s.c.). We measured blood pressure and collected urine and blood for nitric oxide measurement. NO2 was quantified by HPLC. Blood pressure was: control, 97 +/- 7 mmHg; L-NAME, 151 +/- 4.6 mmHg; L-NAME + SnCl2, 133 +/- 3 mmHg, and L-NAME + dexamethasone 152 +/- 4.5 mmHg. Urine nitrite concentration was: 1) 1.832 +/- 0.32, 2) 1.031 +/- 0.23, 3) 1.616 +/- 0.33, and 4) 1.244 +/- 0.33 mumol/mL, while the concentration in blood was: 1) 0.293 +/- 0.06, 2) 0.150 +/- 0.05, 3) 0.373 +/- 0.13, and 4) 0.373 +/- 0.07 mumol/mL. L-NAME + SnCl2 decreased cytochrome P450 renal content, and L-NAME + dexamethasone showed a similar response. In conclusion, both, nitric oxide and CYP-arachidonic acid metabolites play a role in the regulation of blood pressure. Nitric oxide also partially regulates renal cytochrome P450 content.

Participación del óxido nítrico y los metabolitos del ácido araquidónico vía citocromo P450 en la regulación de la presión arterial / Participation of nitric oxide and arachidonic acid metabolites via cytochrome-p450 in the regulation of arterial blood pressure

El óxido nítrico y los metabolitos del ácido araquidónico vía citocromo P450 contribuyen a la regulación de la presión arterial. La modificación en la síntesis de estos autacoides conduce a hipertensión arterial, sin embargo, se desconoce si existe interacción. Por ello, decidimos estudiar el papel modulador del óxido nítrico y los metabolitos del ácido araquidónico vía citocromo P450, y su interacción, sobre la presión arterial y el contenido renal de citocromo P450. Ratas Wistar macho fueron divididas por grupos: 1) Control, 2) L-NAME (100mg/kg/d v.o.), 3) L-NAME + SnCl2 (10mg/kg/d i.p.) y 4) L-NAME + dexametasona (1mg/kg/d s.c.). Se determinó la presión arterial sistólica y la concentración de nitritos por HPLC en orina y sangre. Los valores de presión arterial sistólica fueron: control 97 ± 7 mmHg, L-NAME 151 ± 4.6 mmHg, L-NAME + SnCl2 133 ± 3 mmHg, y L-NAME + dexametasona 152 ± 4.5 mmHg. Los nitritos en orina fueron: 1) 1.832 ± 0.32, 2) 1.031 ± 0.23, 3) 1.616 ± 0.33 y 4) 1.244 ± 0.33 μmol/mL y en sangre: 1) 0.293 ± 0.06, 2) 0.150 ± 0.05, 3) 0.373 ± 0.13 y 4) 0.373 ± 0.07 μmol/mL. El contenido renal de citocromo P450 fue abatido con el tratamiento de L-NAME + SnCl2, y una respuesta semejante se observó con L-NAME + dexametasona. Tanto óxido nítrico como los metabolitos del ácido araquidónico vía CYP participan en la regulación de la presión arterial. Además, el óxido nítrico contribuye regulando parcialmente el contenido renal del citocromo P450.

Nitric oxide and cytochrome P450 arachidonic acid metabolites participate in blood pressure regulation. The synthesis of these autacoids leads to arterial hypertension. However, it is not known whether there is an interaction between them. Therefore, we studied the modulatory effect of nitric oxide and cytochrome P450-arachidonic acid metabolites, their interaction on blood pressure, and the renal content of cytochrome P450. Male Wistar rats were divided: 1) control, 2) L-NAME (100 mg/kg/d p.o.), 3) L-NAME + SnCl2 (10 mg/kg/d i.p.), and 4) L-NAME + dexamethasone (1 mg/kg/d s.c.). We measured blood pressure and collected urine and blood for nitric oxide measurement. NO2 was quantified by HPLC. Blood pressure was: control, 97 ± 7 mmHg; L-NAME, 151 ± 4.6 mmHg; L-NAME + SnCl2, 133 ± 3 mmHg, and L-NAME + dexamethasone 152 ± 4.5 mmHg. Urine nitrite concentration was: 1) 1.832 ± 0.32, 2) 1.031 ± 0.23, 3) 1.616 ± 0.33, and 4) 1.244 ± 0.33 μmol/mL, while the concentration in blood was: 1) 0.293 ± 0.06, 2) 0.150 ± 0.05, 3) 0.373 ± 0.13, and 4) 0.373 ± 0.07 μmol/ mL. L-NAME + SnCl2 decreased cytochrome P450 renal content, and L-NAME + dexamethasone showed a similar response. In conclusion, both, nitric oxide and CYP-arachidonic acid metabolites play a role in the regulation of blood pressure. Nitric oxide also partially regulates renal cytochrome P450 content. (Arch Cardiol Mex 2003; 73:98-104).

Behavior of enterotoxigenic strains of Staphylococcus aureus in milk fermented with a yogurt starter culture.

The ability of a yogurt starter culture formed by Streptococcus salivarius subsp. thermophilus and Lactobacillus delbrueckii subsp bulgaricus to inhibit the growth of four enterotoxin type A and B producers Staphylococcus aureus strains (ATCC 6538, S6, FRI-100 and a strain isolated from milk) during fermentation of milk and subsequent storage was investigated. Sterile skim milk was inoculated with about 10(6) CFU/ml of S. aureus and with about 10(6) CFU of starter culture, and incubated at 42 degrees C during 8 h, followed by refrigeration at 4 degrees C. Samples were taken every 2 h during fermentation and every 2 days during storage. Viable count of lactic acid bacteria and S. aureus as well as pH, acidity, thermostable deoxyribonuclease (TNase) and staphylococcal enterotoxin A (SEA) production were evaluated. Behavior of four strains was similar; S. aureus survived the 8 h fermentation with LAB, and its population began to decrease from the first day of storage, being completely inhibited at 9-10 days. TNase and SEA production were positive in all samples taken along the study. It was demonstrated that enterotoxigenic strains of S. aureus were able to survive the fermentation of milk with a yogurt starter culture and they were inhibited after several days during storage of the fermented product, contrary to the general belief which considered it very difficult due to the low pH. Even though S. aureus was inhibited, TNase and SEA were demonstrable along the storage. Therefore, fermented milks may play an important role in the transmission of this organism.

[Isolation of Staphylococcus aureus by the Baird Parker method from powdered milk]. / Aislamiento de Staphylococcus aureus por el método de Baird Parker a partir de leche en polvo.

There are many media recommended for the isolation of Staphylococcus aureus from foods, but only with some media one can obtain a good growth started with stressed cells. The Baird Parker (BP) medium is considered the best choice to recover stressed cells, however, it is not as good a medium to isolate Staphylococcus aureus from powder milk. Therefore, it is important to count with alternative media to enhance the chance for Staphylococcus aureus to grow from dehydrated products. Thirty-one powder milk samples contaminated with Staphylococcus aureus were analysed by Baird Parker method, employing four culture media: Baird Parker (BP), Baird Parker + tween + MgCl2 (BPTM), Pork plasma with bovine fibrinogen agar (PPF) and Salt Milk agar (SL). Staphylococcus aureus was isolated in SL, 38.7%; in BP, 3.2%; in BPTM, 6.4%; and PPF, 0%.

[Demonstration of staphylococcal thermonuclease from powdered milk]. / Demostración de termonucleasa (TNasa) estafilocócica a partir de leche en polvo.

Demonstration of Staphylococcal Thermonuclease (TNase) from Powder Milk. Some authors have reported that the number of Staphylococcus aureus needed to produce a food-poisoning is 10(6) CFU per gram of food, however, other authors have reported foods without microorganisms but these have produced food-poisoning. Because the methods for staphylococcal enterotoxins demonstration in foods are laborious and expensive procedures, in this paper we tried to demonstrate the thermonuclease (TNase) presence in foods directly, as a helper test for screening foods suspected to be contaminated with this microorganism. To 112 powder milk samples were determined TNase presence by Tatini's et al (1976) and Lachica's (1972) technics, 31 of this samples had S. aureus. Only with Lachica's technique it could be possible to demonstrate TNase in 17 of 112 analyzed samples, 14 of these had viable S. aureus.