Effect of alpha linolenic acid on membrane fluidity and respiration of liver mitochondria in normoglycemic and diabetic Wistar rats.

The omega 3 fatty acids (ω3FA) have been recommended for the treatment of Type 2 Diabetes Mellitus (T2DM) and its complications, but there are studies questioning those beneficial effects. In this research, we supplemented the short-chain ω3FA, alpha-linolenic acid (ALA), to a model of rats with T2DM and normoglycemic controls, for 5 months. We were mainly interested in studying the effects of diabetes and ALA on the physicochemical properties of mitochondrial membranes and the consequences on mitochondrial respiration. We found that the Respiratory Control (RC) of diabetic rats was 46% lower than in control rats; in diabetic rats with ALA supplement, it was only 23.9% lower, but in control rats with ALA supplement, the RC was 29.5% higher, apparently improving. Diabetes also decreased the membrane fluidity, changed the thermotropic characteristics of membranes, and increased the proportion of saturated fatty acids. ALA supplement partially kept regulated the physicochemical properties of mitochondrial membranes in induced rats. Our data indicate that diabetes decreased the membrane fluidity through changes in the fatty acids composition that simultaneously affected the RC, which means that the mitochondrial respiration is highly dependent on the physicochemical properties of the membranes. Simultaneously, it was followed the effects of ALA on the progress of diabetes and we found also that the supplementation of ALA helped in controlling glycaemia in rats induced to T2DM; however, in control non-induced rats, the supplementation of ALA derived in characteristics of initial development of diabetes.

Biphasic effect of alpha-linolenic acid on glucose-induced dysmorphogenesis and lipoperoxidation in whole rat embryo in culture.

Type 1 diabetes mellitus complicated with pregnancy, know as diabetic embryopathy, is the cause of neonatal malformations and low for gestational age neonates. With the use of the whole-embryo culture system, it has been demonstrated that high glucose causes embryo dysmorphogenesis, and that oxidative stress appears to be the main mechanism. In recent years, beneficial effect of omega-3 fatty acids has been demonstrated in various diabetic models, and in diabetic complications. Since diabetic embryopathy is mediated probably through membrane lipoperoxidation, This study was designed to find if omega-3 fatty acids could ameliorate the effect of high glucose over the dysmorphogenesis of whole rat embryo in culture. Postimplantational rat embryos were cultured in hyperglycemic media, with addition of alpha-linolenic acid, and morphologic and morphometric parameters were registered. Also, lipoperoxidation and fatty acids composition were measured in cultured embryos. Growth of embryos cultured in presence of glucose was very affected, whereas lipoperoxidation was increased, and it was found that Triton X-100 causes similar results than glucose. Addition of low micromolar doses of alpha-linolenic acid overcome the effect of high glucose or Triton X-100, but higher doses does not ameliorates the effects of the carbohydrate or the detergent. Paradoxically, there are not significant changes in fatty acids composition, although the U/S fatty acids ratio shows an increasing tendency by high glucose and a normalizing tendency by omega-3 fatty acids. In conclusion, glucose and Triton X-100 induces in vitro dysmorphogenesis in post-implantational rat embryos associated with increased lipoperoxidation; and this nocive effect could be ameliorated by low micromolar doses of ALA.

Liver mitochondrial membrane fluidity at early development of diabetes and its correlation with the respiration.

The biological membranes are important in cell function but, during development of diseases such as diabetes, they are impaired. Consequently, membrane-associated biological processes are impaired as well. The mitochondria are important organelles where oxidative phosphorylation takes place, a process closely related with the membranes. In general, it is accepted that the development process of diabetes decreases membrane fluidity. However, in some cases, it has been found to increase membrane fluidity of mitochondria but to decrease the Respiratory Control (RC) index. In this study we found an increase of membrane fluidity and an increase of the RC at an early phase of the development of a type 2 diabetes model. We measured the lipoperoxidation, analyzed the fatty acids composition by gas chromatography, and assessed membrane fluidity using three fluorescent monitors located at different depths inside the bilayer, dipyrenilpropane (DPyP), diphenylhexatriene (DPH), and trimethylammonium diphenylhexatriene (TMA-DPH). Our findings indicate that in the initial stage of diabetes development, when lipoperoxidation still is not significant, the membrane fluidity of liver mitochondria increases because of the increment in the unsaturated to saturated fatty acids ratio (U/S), thus producing an increase of the RC. The membrane fluidity is not the same at all depths in the bilayer. Contrary to the results obtained in mitochondria, the diabetes induced a decrease in the U/S fatty acids ratio of liver total lipids, indicating that the mitochondria might have an independent mechanism for regulating its fatty acids composition.

Avocado oil induces long-term alleviation of oxidative damage in kidney mitochondria from type 2 diabetic rats by improving glutathione status.

Hyperglycemia and mitochondrial ROS overproduction have been identified as key factors involved in the development of diabetic nephropathy. This has encouraged the search for strategies decreasing glucose levels and long-term improvement of redox status of glutathione, the main antioxidant counteracting mitochondrial damage. Previously, we have shown that avocado oil improves redox status of glutathione in liver and brain mitochondria from streptozotocin-induced diabetic rats; however, the long-term effects of avocado oil and its hypoglycemic effect cannot be evaluated because this model displays low survival and insulin depletion. Therefore, we tested during 1 year the effects of avocado oil on glycemia, ROS levels, lipid peroxidation and glutathione status in kidney mitochondria from type 2 diabetic Goto-Kakizaki rats. Diabetic rats exhibited glycemia of 120-186 mg/dL the first 9 months with a further increase to 250-300 mg/dL. Avocado oil decreased hyperglycemia at intermediate levels between diabetic and control rats. Diabetic rats displayed augmented lipid peroxidation and depletion of reduced glutathione throughout the study, while increased ROS generation was observed at the 3rd and 12th months along with diminished content of total glutathione at the 6th and 12th months. Avocado oil ameliorated all these defects and augmented the mitochondrial content of oleic acid. The beneficial effects of avocado oil are discussed in terms of the hypoglycemic effect of oleic acid and the probable dependence of glutathione transport on lipid peroxidation and thiol oxidation of mitochondrial carriers.

Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats.

Electron transport chain (ETC) dysfunction, excessive ROS generation and lipid peroxidation are hallmarks of mitochondrial injury in the diabetic liver, with these alterations also playing a role in the development of non-alcoholic fatty liver disease (NAFLD). Enhanced mitochondrial sensitivity to lipid peroxidation during diabetes has been also associated to augmented content of C22:6 in membrane phospholipids. Thus, we aimed to test whether avocado oil, a rich source of C18:1 and antioxidants, attenuates the deleterious effects of diabetes on oxidative status of liver mitochondria by decreasing unsaturation of acyl chains of membrane lipids and/or by improving ETC functionality and decreasing ROS generation. Streptozocin-induced diabetes elicited a noticeable increase in the content of C22:6, leading to augmented mitochondrial peroxidizability index and higher levels of lipid peroxidation. Mitochondrial respiration and complex I activity were impaired in diabetic rats with a concomitant increase in ROS generation using a complex I substrate. This was associated to a more oxidized state of glutathione, All these alterations were prevented by avocado oil except by the changes in mitochondrial fatty acid composition. Avocado oil did not prevented hyperglycemia and polyphagia although did normalized hyperlipidemia. Neither diabetes nor avocado oil induced steatosis. These results suggest that avocado oil improves mitochondrial ETC function by attenuating the deleterious effects of oxidative stress in the liver of diabetic rats independently of a hypoglycemic effect or by modifying the fatty acid composition of mitochondrial membranes. These findings might have also significant implications in the progression of NAFLD in experimental models of steatosis.

Dietary avocado oil supplementation attenuates the alterations induced by type I diabetes and oxidative stress in electron transfer at the complex II-complex III segment of the electron transport chain in rat kidney mitochondria.

Impaired complex III activity and reactive oxygen species (ROS) generation in mitochondria have been identified as key events leading to renal damage during diabetes. Due to its high content of oleic acid and antioxidants, we aimed to test whether avocado oil may attenuate the alterations in electron transfer at complex III induced by diabetes by a mechanism related with increased resistance to lipid peroxidation. 90 days of avocado oil administration prevented the impairment in succinate-cytochrome c oxidoreductase activity caused by streptozotocin-induced diabetes in kidney mitochondria. This was associated with a protection against decreased electron transfer through high potential chain in complex III related to cytochromes c + c1 loss. During Fe(2+)-induced oxidative stress, avocado oil improved the activities of complexes II and III and enhanced the protection conferred by a lipophilic antioxidant against damage by Fe(2+). Avocado oil also decreased ROS generation in Fe(2+)-damaged mitochondria. Alterations in the ratio of C20:4/C18:2 fatty acids were observed in mitochondria from diabetic animals that not were corrected by avocado oil treatment, which yielded lower peroxidizability indexes only in diabetic mitochondria although avocado oil caused an augment in the total content of monounsaturated fatty acids. Moreover, a protective effect of avocado oil against lipid peroxidation was observed consistently only in control mitochondria. Since the beneficial effects of avocado oil in diabetic mitochondria were not related to increased resistance to lipid peroxidation, these effects were discussed in terms of the antioxidant activity of both C18:1 and the carotenoids reported to be contained in avocado oil.

Avocado oil alleviates non-alcoholic fatty liver disease by improving mitochondrial function, oxidative stress and inflammation in rats fed a high fat-High fructose diet.

Non-alcoholic fatty liver disease (NAFLD) is characterized by lipid accumulation in hepatocytes, and in advanced stages, by inflammation and fibrosis. Excessive ROS production due to mitochondrial dysfunction contributes to NAFLD development, making the decrease in mitochondrial ROS production an emerging target to alleviate NAFLD. Previously, we have shown that avocado oil, a source of several bioactive compounds with antioxidant effects, decreases oxidative stress by improving the function of the mitochondrial electron transport chain (ETC) and decreasing ROS levels in mitochondria of diabetic and hypertensive rats. Therefore, we tested in this work whether avocado oil alleviates NAFLD by attenuating mitochondrial dysfunction, oxidative stress and inflammation. NAFLD was induced in rats by a high fat-high fructose (HF) diet administered for six (HF6) or twelve (HF12) weeks. Hepatic steatosis, hypertrophy and inflammation were detected in both the HF6 and HF12 groups. Hyperglycemia was observed only in the HF12 group. The HF6 and HF12 groups displayed dyslipidemia, impairments in mitochondrial respiration, complex III activity, and electron transfer in cytochromes in the complex III. This led to an increase in the levels of ROS and lipid peroxidation. The substitution of the HF6 diet by standard chow and avocado oil for 6 weeks (HF6+AVO + D), or supplementation of the HF12 diet with avocado oil (HF12 + AVO), ameliorated NAFLD, hyperglycemia, dyslipidemia, and counteracted mitochondrial dysfunctions and oxidative stress. The substitution of the HF6 diet by standard chow without avocado oil did not correct many of these abnormalities, confirming that the removal of the HF diet is not enough to counteract NAFLD and mitochondrial dysfunction. In summary, avocado oil decreases NAFLD by improving mitochondrial function, oxidative stress, and inflammation.

Electron transport chain dysfunction by H(2)O (2) is linked to increased reactive oxygen species production and iron mobilization by lipoperoxidation: studies using Saccharomyces cerevisiae mitochondria.

The mitochondrial electron transport chain (ETC) contains thiol groups (-SH) which are reversibly oxidized to modulate ETC function during H(2)O(2) overproduction. Since deleterious effects of H(2)O(2) are not limited to -SH oxidation, due to the formation of other H(2)O(2)-derived species, some processes like lipoperoxidation could enhance the effects of H(2)O(2) over ETC enzymes, disrupt their modulation by -SH oxidation and increase superoxide production. To verify this hypothesis, we tested the effects of H(2)O(2) on ETC activities, superoxide production and iron mobilization in mitochondria from lipoperoxidation-resistant native yeast and lipoperoxidation-sensitized yeast. Only complex III activity from lipoperoxidation-sensitive mitochondria exhibited a higher susceptibility to H(2)O(2) and increased superoxide production. The recovery of ETC activity by the thiol reductanct ß-mercaptoethanol (BME) was also altered at complex III, and a role was attributed to lipoperoxidation, the latter being also responsible for iron release. A hypothetical model linking lipoperoxidation, increased complex III damage, superoxide production and iron release is given.

Effect of phosphatidylcholine-cholesterol liposomes on Entamoeba histolytica virulence.

Trophozoites of Entamoeba histolytica HM-1:IMSS become less virulent after long-term maintenance in axenic cultures. The factors responsible for the loss of virulence during in vitro cultivation remain unclear. However, it is known that in vitro cultivation of amoeba in culture medium supplemented with cholesterol restores their virulence. In this study, we analyzed the effect of adding phosphatidylcholine-cholesterol (PC-Chol) liposomes to the culture medium and evaluated the effect of this lipid on various biochemical and biological functions of E. histolytica HM-1:IMSS in terms of its virulence. The addition of PC-Chol liposomes to the culture medium maintained the virulence of these parasites against hamster liver at the same level as the original virulent E. histolytica strain, even though these amoebae were maintained without passage through hamster liver for 18 months. The trophozoites also showed increased endocytosis, erythrophagocytosis, and carbohydrate residue expression on the amoebic surface. Protease activities were also modified by the presence of cholesterol in the culture medium. These findings indicate the capacity of cholesterol to preserve amoeba virulence and provide an alternative method for the maintenance of virulent E. histolytica trophozoites without the need for in vivo procedures.

Elucidation of the effects of lipoperoxidation on the mitochondrial electron transport chain using yeast mitochondria with manipulated fatty acid content.

Lipoperoxidative damage to the respiratory chain proteins may account for disruption in mitochondrial electron transport chain (ETC) function and could lead to an augment in the production of reactive oxygen species (ROS). To test this hypothesis, we investigated the effects of lipoperoxidation on ETC function and cytochromes spectra of Saccharomyces cerevisiae mitochondria. We compared the effects of Fe(2+) treatment on mitochondria isolated from yeast with native (lipoperoxidation-resistant) and modified (lipoperoxidation-sensitive) fatty acid composition. Augmented sensitivity to oxidative stress was observed in the complex III-complex IV segment of the ETC. Lipoperoxidation did not alter the cytochromes content. Under lipoperoxidative conditions, cytochrome c reduction by succinate was almost totally eliminated by superoxide dismutase and stigmatellin. Our results suggest that lipoperoxidation impairs electron transfer mainly at cytochrome b in complex III, which leads to increased resistance to antimycin A and ROS generation due to an electron leak at the level of the Q(O) site of complex III.

Bcl-2 expression in a diabetic embryopathy model in presence of polyamines.

The frequency of congenital malformations is 3-5 times higher in mothers with pregestational diabetes mellitus than in general population. Apparently, this problem is due to change in the expression of apoptotic and antiapoptotic genes induced by the oxidative stress derived from the diabetes/hyperglycemia. One of these genes is Bcl-2, which is associated with the control and inhibition of apoptosis. The purpose of the present work was to study the effect of polyamine addition over expression of Bcl-2 gene in a model of diabetic embryopathy. For this, gestational day 10.5 (GD10.5) rat embryos were incubated at 37°C for 24 h in control medium, medium with high glucose, or medium with high glucose and supplemented with spermidine or spermine. Post-cultured embryos were harvested and observed to obtain morphological scores; some of them were subjected to molecular biology studies: DNA isolation plus conventional PCR or RNA isolation plus RT-PCR; other embryos were fixed with paraformaldehyde and used for immunohistochemical detection of Bcl-2 protein. Although Bcl-2 mRNA was similarly expressed in all rat embryo treatments, Bcl-2 protein was found only in control-incubated embryos. In conclusion, it seems that the inhibition of Bcl-2 gene expression induced by glucose was not reversed by polyamines.

El artículo científico: de la recepción del manuscrito a su publicación

El trabajo editorial casi nunca es visible en la cadena de la transmisión del conocimiento; sin embargo, es una tarea ardua, exhaustiva y precisa, en la evaluación, selección, producción y distribución del material científico, además de su difusión y marketing. Es por ello que en los siguientes párrafos se explicará, de manera sencilla, cómo es que el saber científico se construye, difunde y crea un nuevo saber, gracias a las editoriales y sus profesionales. Todo esfuerzo creador en el área de la ciencia debe tener constancia mediante un escrito, por ende, el objetivo del trabajo fue resumir el proceso de la creación del artículo científico desde la recepción del manuscrito hasta su publicación. Para ello se utilizó el método de la revisión narrativa. El artículo científico, como procedimiento individual o gremial para la difusión del desarrollo e innovación, ha sido el más empleado para mostrar el conocimiento novedoso, conservar el más antiguo y lograr que la información llegue a sus destinatarios, los cuales no necesariamente son generadores del saber humano, pero sí difusores. La descripción, evaluación y divulgación de la ciencia (socialización de la ciencia) ha sido un aspecto esencial en el desarrollo tecno-científico, que cuenta con medios certificados (revistas científicas) para acreditar y validar el conocimiento que se ha generado, o está en proceso, en un campo determinado, período de tiempo y región específicos.

Editorial work is almost never visible in the knowledge transmission chain; however, it is an arduous, exhaustive and precise task, in evaluating, selecting, producing and distributing scientific material, as well as its dissemination and marketing. That is why the following paragraphs will explain, in a simple way, how scientific knowledge is built, disseminated and creates new knowledge, thanks to publishers and their professionals. Every creative effort in the area of science must be recorded in writing, therefore, the objective of the work was to summarize the process of creating the scientific article since the reception of the manuscript to its publication; to this end, the narrative review method was used. The scientific article, as an separate or union procedure for the dissemination of development and innovation, has been the most used to show new knowledge, to preserve the first and to ensure that the information reaches its recipients, who are not necessarily generators of human knowledge, but diffusers. The description, evaluation and dissemination of science (socialization of science) has been an essential aspect in the techno-scientific development, which has certified means (scientific journals) to accredit and validate the knowledge that has been generated, or it is in progress, in a certain field, a given period and a specific region.

Oxidative stress and antioxidant response in a thermotolerant yeast.

Stress tolerance is a key attribute that must be considered when using yeast cells for industrial applications. High temperature is one factor that can cause stress in yeast. High environmental temperature in particular may exert a natural selection pressure to evolve yeasts into thermotolerant strains. In the present study, three yeasts (Saccharomyces cerevisiae, MC4, and Kluyveromyces marxianus, OFF1 and SLP1) isolated from hot environments were exposed to increased temperatures and were then compared with a laboratory yeast strain. Their resistance to high temperature, oxidative stress, and antioxidant response were evaluated, along with the fatty acid composition of their cell membranes. The SLP1 strain showed a higher specific growth rate, biomass yield, and biomass volumetric productivity while also showing lower duplication time, reactive oxygen species (ROS) production, and lipid peroxidation. In addition, the SLP1 strain demonstrated more catalase activity after temperature was increased, and this strain also showed membranes enriched in saturated fatty acids. It is concluded that the SLP1 yeast strain is a thermotolerant yeast with less oxidative stress and a greater antioxidant response. Therefore, this strain could be used for fermentation at high temperatures.

Endothelium-dependent inhibition of the contractile response is decreased in aorta from aged and spontaneously hypertensive rats.

BACKGROUND: Stimulation of vascular 5-hydroxytryptamine-2C (5-HT(2c)) receptors produces contraction in rat aorta. We investigated the effect of aging on endothelium-dependent inhibition of contractile responses in thoracic aorta from normotensive Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR). METHODS: Endothelium-intact and denuded aortic rings were prepared from young (7-9 weeks old) and senescent (65-70 weeks old) WKY and SHR rats. Changes in isometric tension elicited by 5-HT, in the absence or in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME) or indomethacin were recorded. RESULTS: In aorta from WKY and SHR, 5-HT elicited concentration-dependent contractions, which were increased by endothelium removal. The ability of endothelium to depress contractile response to 5-HT was found to be reduced in vessels from senescent animals, mainly in SHR. L-NAME increased the sensitivity and maximal effect to 5-HT in endothelium-intact but not in denuded aortic rings from young WKY rats. The effect of L-NAME was lower in young SHR compared with age-matched WKY rats, but it did not modify the response to 5-HT in senescent rats. Indomethacin did not affect contraction in arteries from young WKY or in denuded aortic rings from young SHR and aged WKY. In contrast, the inhibitor attenuated the response in endothelium-intact vessels from young SHR and aged WKY, and this effect was more marked in arteries with and without endothelium from senescent SHR. Thus, inhibition of cyclooxygenases by indomethacin revealed an enhanced endothelium-dependent modulation of contraction in senescent and hypertensive rats. CONCLUSIONS: Results indicate that hypertension and aging decrease the negative modulator role of endothelium, in 5-HT-induced vasoconstriction in aorta from WKY and SHR. Data also point out that endothelial dysfunction involves an increased formation of vasoconstrictor prostanoids, which counteract nitric oxide effects. In addition, SHR endothelium releases contractile prostanoids at an early stage of hypertension, whereas in old SHR vascular smooth muscle also releases prostanoids, which contribute to 5-HT-induced contraction.

Even a Chronic Mild Hyperglycemia Affects Membrane Fluidity and Lipoperoxidation in Placental Mitochondria in Wistar Rats.

It is known the deleterious effects of diabetes on embryos, but the effects of diabetes on placenta and its mitochondria are still not well known. In this work we generated a mild hyperglycemia model in female wistar rats by intraperitoneal injection of streptozotocin in 48 hours-old rats. The sexual maturity onset of the female rats was delayed around 6-7 weeks and at 16 weeks-old they were mated, and sacrificed at day 19th of pregnancy. In placental total tissue and isolated mitochondria, the fatty acids composition was analyzed by gas chromatography, and lipoperoxidation was measured by thiobarbituric acid reactive substances. Membrane fluidity in mitochondria was measured with the excimer forming probe dipyrenylpropane and mitochondrial function was measured with a Clark-type electrode. The results show that even a chronic mild hyperglycemia increases lipoperoxidation and decreases mitochondrial function in placenta. Simultaneously, placental fatty acids metabolism in total tissue is modified but in a different way than in placental mitochondria. Whereas the chronic mild hyperglycemia induced a decrease in unsaturated to saturated fatty acids ratio (U/S) in placental total tissue, the ratio increased in placental mitochondria. The measurements of membrane fluidity showed that fluidity of placenta mitochondrial membranes increased with hyperglycemia, showing consistency with the fatty acids composition through the U/S index. The thermotropic characteristics of mitochondrial membranes were changed, showing lower transition temperature and activation energies. All of these data together demonstrate that even a chronic mild hyperglycemia during pregnancy of early reproductive Wistar rats, generates an increment of lipoperoxidation, an increase of placental mitochondrial membrane fluidity apparently derived from changes in fatty acids composition and consequently, mitochondrial malfunction.

Change in lipoperoxidation but not in scavenging enzymes activity during polyamine embryoprotection in rat embryo cultured in hyperglycemic media.

DM1 complicated with pregnancy is the cause of neonatal malformations and low-for-gestational-age neonates. With the use of the whole-embryo culture system, it has been demonstrated that high glucose causes embryo dysmorphogenesis. Previously, our group has found that spermidine or spermine addition reverts almost fully the severity and frequency of dysmorphogenesis, whereas the effect of arginine and putrescine it is only partial. A hypothesis for polyamine mechanism is the amelioration of oxidative stress caused by high glucose. The purpose of this work was to evaluate the effect of polyamines over the activity of scavenging enzymes and lipoperoxidation in whole-embryo rat in culture. Post-implantation (gestational day 10.5) rat embryos were cultured for 24 h in normal medium or hyperglycemic medium, alone or supplemented with L-arginine or polyamine. Embryos were recovered and visualized, and morphologic parameters were registered. Cultured embryos were homogenized, and superoxide dismutase and glutathione-reductase activities, as well as lipoperoxidation, were measured. The activity of superoxide dismutase and glutathione peroxidase were not affected by the treatment, but lipoperoxidation was increased in embryos cultured in hyperglycemic medium; spermidine or spermine supplementation restore lipoperoxidation to near-normal values, and putrescine and L-arginine reverts only partially the glucose effect. Taken together, these results pointed out that spermidine and spermine embryoprotection could be mediated by direct antioxidant activity. However, further studies are needed to support this hypothesis.

Oxidative stress and antioxidant response in a thermotolerant yeast

Abstract Stress tolerance is a key attribute that must be considered when using yeast cells for industrial applications. High temperature is one factor that can cause stress in yeast. High environmental temperature in particular may exert a natural selection pressure to evolve yeasts into thermotolerant strains. In the present study, three yeasts (Saccharomyces cerevisiae, MC4, and Kluyveromyces marxianus, OFF1 and SLP1) isolated from hot environments were exposed to increased temperatures and were then compared with a laboratory yeast strain. Their resistance to high temperature, oxidative stress, and antioxidant response were evaluated, along with the fatty acid composition of their cell membranes. The SLP1 strain showed a higher specific growth rate, biomass yield, and biomass volumetric productivity while also showing lower duplication time, reactive oxygen species (ROS) production, and lipid peroxidation. In addition, the SLP1 strain demonstrated more catalase activity after temperature was increased, and this strain also showed membranes enriched in saturated fatty acids. It is concluded that the SLP1 yeast strain is a thermotolerant yeast with less oxidative stress and a greater antioxidant response. Therefore, this strain could be used for fermentation at high temperatures.

Analysis of the membrane fluidity of erythrocyte ghosts in diabetic, spontaneously hypertensive rats.

Diabetes and hypertension are closely related diseases associated with changes in membrane fluidity. Here, we measured the membrane fluidity of erythrocyte ghosts from spontaneously hypertensive rats (SHR), with or without streptozotocin (STZ)-induced diabetes, at the ages of 1, 3 and 6 months, by introducing the use of the intramolecular excimer forming dipyrenylpropane (DPyP) in this model. Type 2 diabetes mellitus (T2DM) was induced in 48-h-old, newborn male SHR by intraperitoneal injection of STZ. We found lower excimer to monomer (I (e)/I (m)) DPyP ratios in diabetic SHR than in control SHR at 3 and 6 months old, indicating a decrease in membrane fluidity. Simultaneously, the composition of fatty acids was determined and it was found that the unsaturated to saturated fatty acids ratio (U/S) was compatible with changes in membrane fluidity. These results suggest that the change in fatty acid composition of erythrocyte ghosts contributes significantly to the decreased membrane fluidity detected with DPyP in diabetic SHR.