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1.
Yeast ; 39(11-12): 617-628, 2022 11.
Article in English | MEDLINE | ID: mdl-36285422

ABSTRACT

Quercetin is a flavonol ubiquitously present in fruits and vegetables that shows a potential therapeutic use in non-transmissible chronic diseases, such as cancer and diabetes. Although this phytochemical has shown promising health benefits, the molecular mechanism behind this compound is still unclear. Interestingly, quercetin displays toxic properties against phylogenetically distant organisms such as bacteria and eukaryotic cells, suggesting that its molecular target resides on a highly conserved pathway. The cytotoxicity of quercetin could be explained by energy depletion occasioned by mitochondrial respiration impairment and its concomitant pleiotropic effect. Thereby, the molecular basis of quercetin cytotoxicity could shed light on potential molecular mechanisms associated with its health benefits. Nonetheless, the evidence supporting this hypothesis is still lacking. Thus, this study aimed to evaluate whether quercetin supplementation affects mitochondrial respiration and whether this is related to quercetin cytotoxicity. Saccharomyces cerevisiae was used as a study model to assess the effect of quercetin on energetic metabolism. Herein, we provide evidence that quercetin supplementation: (1) decreased the exponential growth of S. cerevisiae in a glucose-dependent manner; (2) affected diauxic growth in a similar way to antimycin A (complex III inhibitor of electron transport chain); (3) suppressed the growth of S. cerevisiae cultures supplemented with non-fermentable carbon sources (glycerol and lactate); (4) promoted a glucose-dependent inhibition of the basal, maximal, and ATP-linked respiration; (5) diminished complex II and IV activities. Altogether, these data indicate that quercetin disturbs mitochondrial respiration between the ubiquinone pool and cytochrome c, and this phenotype is associated with its cytotoxic properties.


Subject(s)
Quercetin , Saccharomyces cerevisiae , Saccharomyces cerevisiae/metabolism , Quercetin/pharmacology , Quercetin/metabolism , Mitochondria/metabolism , Glucose/metabolism , Respiration
2.
Yeast ; 39(3): 193-207, 2022 03.
Article in English | MEDLINE | ID: mdl-34693568

ABSTRACT

The antioxidant phenotype caused by resveratrol has been recognized as a key piece in the health benefits exerted by this phytochemical in diseases related to aging. It has recently been proposed that a mitochondrial pro-oxidant mechanism could be the cause of resveratrol antioxidant properties. In this regard, the hypothesis that resveratrol impedes electron transport to complex III of the electron transport chain as its main target suggests that resveratrol could increase reactive oxygen species (ROS) generation through reverse electron transport or by the semiquinones formation. This idea also explains that cells respond to resveratrol oxidative damage, inducing their antioxidant systems. Moreover, resveratrol pro-oxidant properties could accelerate the aging process, according to the free radical theory of aging, which postulates that organism's age due to the accumulation of the harmful effects of ROS in cells. Nonetheless, there is no evidence linking the chronological lifespan (CLS) shorten occasioned by resveratrol with a pro-oxidant mechanism. Hence, this study aimed to evaluate whether resveratrol shortens the CLS of Saccharomyces cerevisiae due to a pro-oxidant activity. Herein, we provide evidence that supplementation with 100 µM of resveratrol at 5% glucose: (1) shortened the CLS of ctt1Δ and yap1Δ strains; (2) decreased ROS levels and increased the catalase activity in WT strain; (3) maintained unaffected the ROS levels and did not change the catalase activity in ctt1Δ strain; and (4) lessened the exponential growth of ctt1Δ strain, which was restored with the adding of reduced glutathione. These results indicate that resveratrol decreases CLS by a pro-oxidant mechanism.


Subject(s)
Longevity , Saccharomyces cerevisiae , Antioxidants/pharmacology , Catalase/metabolism , Catalase/pharmacology , Glucose/pharmacology , Longevity/genetics , Oxidative Stress , Reactive Oxygen Species , Resveratrol/pharmacology , Saccharomyces cerevisiae/genetics
3.
J Food Sci ; 82(6): 1423-1432, 2017 Jun.
Article in English | MEDLINE | ID: mdl-28493309

ABSTRACT

Fresh meat is a highly perishable food. This work aimed to evaluate the influence of Mexican oregano (Lippia graveolens Kunth) incorporated into active coatings (ACs) spread on fresh pork meat as free (FEO), nanoemulsified (NEO), and microencapsulated (MEO) essential oil (EO), on its microbiological, physicochemical and sensory properties during 15 d at 4 ± 1 °C. Thymol and γ-terpinene were identified in the EO. In vitro effect of 2.85 mg EO/cm2 was tested against Brochothrix thermosphacta, Micrococcus luteus, Lactobacillus plantarum, Pseudomonas fragi, and Salmonella Infantis. FEO antioxidant capacity (DPPH assay) was significantly higher than that of thymol, NEO and MEO (93.53%, 89.92%, 77.79%, and 78.50% inhibition, respectively), and similar to BHA (96.03%) and gallic acid (95.57%). FEO, NEO, and MEO ACs on meat caused growth inhibition of lactic acid bacteria (5 log population reduction) and Pseudomonas spp. (4 log reduction), whereas ≤1.5 log population reduction was observed for B. thermosphacta and Salmonella Infantis. Meat microbiota was more efficiently controlled by MEO than by FEO or NEO. ACs delayed lipid and oxymyoglobin oxidation of fresh pork meat. After 15 d of cold storage meat added with EO coatings was desirable for panelists, whereas untreated (UT) samples were undesirable. Active coatings are a significant alternative method for fresh meat preservation.


Subject(s)
Food Microbiology , Lippia/chemistry , Oils, Volatile/pharmacology , Plant Oils/pharmacology , Red Meat/microbiology , Animals , Drug Compounding , Food Preservation/methods , Humans , Mexico , Nanotechnology , Oils, Volatile/chemistry , Plant Oils/chemistry , Swine
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