Efectos de la inclusión dietaría de Ulva clathrata sobre el desempeño reproductivo y la calidad del desove en camarón blanco Litopenaeus vannamei (BOONE, 1931) en condiciones de producción comercial.

En el presente estudio se evaluó el efecto de la suplementación de harina de alga Ulva clathrata en el calamar (20g de harina de Ulva por kg de calamar fresco) de una dieta fresca para maduración de reproductores Litopenaeus vannamei sobre el rendimiento reproductivo, la histología e histoquímica de la gónada, la composición bioquímica, el perfil de ácidos grasos, los esteroles, el contenido de carotenoides y compuestos fenólicos de gónadas, espermatóforos, hepatopáncreas, músculos, huevos y nauplios. Además, se evaluó el agotamiento reproductivo en hembras y la melanización en machos. El estudio se realizó en un laboratorio comercial (Larvas Granmar, La Paz, Baja California Sur) donde se usaron hembras ablacionadas y marcadas con anillos oculares para un seguimiento individual. La evaluación sobre el rendimiento reproductivo mostro que el consumo de Ulva aumentó 17.9% la producción de nauplios por hembra, mejoro 13.3% la tasa de eclosión y disminuyó significativamente la mortalidad (1.11 vs. 2.25 hembras/día/tanque, en comparación con el control) y el agotamiento reproductivo ocasionado por desoves múltiples, al mantener la producción continua de nauplios en hembras con uno o más desoves durante el periodo experimental. Las hembras alimentadas con Ulva tuvieron ovocitos vitelogénicos tardíos y postvitelogénicos más grandes (+7, +15%, respectivamente), y los ovocitos presentaron un área ocupada barras corticales mayor. Las hembras alimentadas con Ulva tuvieron 35% más de lípidos en las gónadas, y 84% más de 20:4n-6 en los acilglicéridos de las gónadas maduras y 30% más de 18:3n-3, 13% de 20:4n-6 y 10% de 22:6n-3 en los fosfolípidos de las gónadas maduras en comparación con los controles. En hepatopáncreas el 22:6n-3 aumentó 51% en los lípidos de reserva en hembras alimentadas con Ulva en comparación con los controles. Los carotenoides aumentaron 43% en las gónadas y cinco veces en el hepatopáncreas en hembras maduras alimentadas con Ulva. La proporción de fucosterol e isofucosterol pasó de indetectable en controles a 0.3 y 0.2%, respectivamente, en camarones alimentados con el alga. Los compuestos fenólicos en la gónada fueron más altos en las gónadas maduras en comparación con los inmaduros, sin embargo, no se encontraron diferencias significativas en relación con el consumo de Ulva

Circadian and non-circadian melatonin: Influence on glucose metabolism in cancer cells

This review considers the role of melatonin as an oncostatic agent and particularly as to how it relates to the mechanisms by which melatonin regulates glucose metabolism in cancer cells. Many tumor cells adopt a means of glucose utilization that is different from that of normal cells. Thus, these cancer cells rapidly take up and metabolize glucose and after it is converted to pyruvate, they accelerate the production of lactate which is abundantly released into the circulation. The change in metabolism that cancer cells makes is referred to as the Warburg effect, or aerobic glycolysis. The switch to aerobic glycolysis affords cancer cells major advantages in terms of an accelerated rate of ATP production and the synthesis of abundant molecular building blocks required for rapid proliferation, invasion, and metastasis. In normal cells, the bulk of the pyruvate formed is shunted into the mitochondria for conversion to acetyl-CoA. Melatonin forces cancer cells to abandon aerobic glycolysis and function with a normal cell phenotype. The oncostatic agent, melatonin, does this by upregulating the enzyme, pyruvate dehydrogenase complex, that ensures pyruvate to acetyl-CoA metabolism; this is presumably achieved by the direct or indirect inhibition of pyruvate dehydrogenase kinase, which normally downregulates pyruvate dehydrogenase complex. By depriving cancer cells of aerobic glycolysis, melatonin converts them to a normal cell phenotype which reduces the rapid cell proliferation and aggressive nature of cancer cells.Fil: Reiter, Russel. University Of Lodz; ArgentinaFil: Sharma, Ramaswamy. No especifíca;Fil: Ma, Qiang. No especifíca;Fil: Rosales Corral, Sergio. Instituto Mexicano del Seguro Social; MéxicoFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentin

Ceremonias de el imperial y militar Colegio de Calatrava : conforme a sus establecimientos, y leyes, a las que se practican en los demas colegios de esta Universidad de Salamanca, y à las Reglas, que han parecido mas conducentes para su exacto regimen, sincèra politica, y acertado gobierno

Copia digital. Valladolid : Junta de Castilla y León. Consejería de Cultura y Turismo, 2009-2010Port. enmarcada en orla tip. xil. y con grab. xil. en rojo (cruz de Calatrava

Diabetes and Alzheimer Disease, Two Overlapping Pathologies with the Same Background: Oxidative Stress

There are several oxidative stress-related pathways interconnecting Alzheimer’s disease and type II diabetes, two public health problems worldwide. Coincidences are so compelling that it is attractive to speculate they are the same disorder. However, some pathological mechanisms as observed in diabetes are not necessarily the same mechanisms related to Alzheimer’s or the only ones related to Alzheimer’s pathology. Oxidative stress is inherent to Alzheimer’s and feeds a vicious cycle with other key pathological features, such as inflammation and Ca2+ dysregulation. Alzheimer’s pathology by itself may lead to insulin resistance in brain, insulin resistance being an intervening variable in the neurodegenerative disorder. Hyperglycemia and insulin resistance from diabetes, overlapping with the Alzheimer’s pathology, aggravate the progression of the neurodegenerative processes, indeed. But the same pathophysiological background is behind the consequences, oxidative stress. We emphasize oxidative stress and its detrimental role in some key regulatory enzymes

Melatonin, a Full Service Anti-Cancer Agent: Inhibition of Initiation, Progression and Metastasis

There is highly credible evidence that melatonin mitigates cancer at the initiation, progression and metastasis phases. In many cases, the molecular mechanisms underpinning these inhibitory actions have been proposed. What is rather perplexing, however, is the large number of processes by which melatonin reportedly restrains cancer development and growth. These diverse actions suggest that what is being observed are merely epiphenomena of an underlying more fundamental action of melatonin that remains to be disclosed. Some of the arresting actions of melatonin on cancer are clearly membrane receptor-mediated while others are membrane receptor-independent and involve direct intracellular actions of this ubiquitously-distributed molecule. While the emphasis of melatonin/cancer research has been on the role of the indoleamine in restraining breast cancer, this is changing quickly with many cancer types having been shown to be susceptible to inhibition by melatonin. There are several facets of this research which could have immediate applications at the clinical level. Many studies have shown that melatonin’s co-administration improves the sensitivity of cancers to inhibition by conventional drugs. Even more important are the findings that melatonin renders cancers previously totally resistant to treatment sensitive to these same therapies. Melatonin also inhibits molecular processes associated with metastasis by limiting the entrance of cancer cells into the vascular system and preventing them from establishing secondary growths at distant sites. This is of particular importance since cancer metastasis often significantly contributes to death of the patient. Another area that deserves additional consideration is related to the capacity of melatonin in reducing the toxic consequences of anti-cancer drugs while increasing their efficacy. Although this information has been available for more than a decade, it has not been adequately exploited at the clinical level. Even if the only beneficial actions of melatonin in cancer patients are its ability to attenuate acute and long-term drug toxicity, melatonin should be used to improve the physical wellbeing of the patients. The experimental findings, however, suggest that the advantages of using melatonin as a co-treatment with conventional cancer therapies would far exceed improvements in the wellbeing of the patients.Shun-Fa Yang, Grant #CHS-2016-E-002-Y2

Melatonin and pathological cell interactions: mitochondrial glucose processing in cancer cells

Melatonin is synthesized in the pineal gland at night. Since melatonin is produced in the mitochondria of all other cells in a non-circadian manner, the amount synthesized by the pineal gland is less than 5% of the total. Melatonin produced in mitochondria influences glucose metabolism in all cells. Many pathological cells adopt aerobic glycolysis (Warburg effect) in which pyruvate is excluded from the mitochondria and remains in the cytosol where it is metabolized to lactate. The entrance of pyruvate into the mitochondria of healthy cells allows it to be irreversibly decarboxylated by pyruvate dehydrogenase (PDH) to acetyl coenzyme A (acetyl-CoA). The exclusion of pyruvate from the mitochondria in pathological cells prevents the generation of acetyl-CoA from pyruvate. This is relevant to mitochondrial melatonin production, as acetyl-CoA is a required co-substrate/co-factor for melatonin synthesis. When PDH is inhibited during aerobic glycolysis or during intracellular hypoxia, the deficiency of acetyl-CoA likely prevents mitochondrial melatonin synthesis. When cells experiencing aerobic glycolysis or hypoxia with a diminished level of acetyl-CoA are supplemented with melatonin or receive it from another endogenous source (pineal-derived), pathological cells convert to a more normal phenotype and support the transport of pyruvate into the mitochondria, thereby re-establishing a healthier mitochondrial metabolic physiology.Fil: Reiter, Russel. University Of Texas At San Antonio. University Of Texas Health Science Center At San Antonio (ut Health San Antonio); Estados UnidosFil: Sharma, Ramaswamy. University Of Texas At San Antonio. University Of Texas Health Science Center At San Antonio (ut Health San Antonio); Estados UnidosFil: Rosales Corral, Sergio. Instituto Mexicano del Seguro Social; MéxicoFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; ArgentinaFil: Almeida Chuffa, Luiz Gustavo de. Institute of Biosciences of Botucatu; BrasilFil: Pires de Campos Zuccari, Debora Aparecida. Faculdade de Medicina de Sao Jose Do Rio Preto; Brasi

Alterations in Lipid Levels of Mitochondrial Membranes Induced by Amyloid-β: A Protective Role of Melatonin

Alzheimer pathogenesis involves mitochondrial dysfunction, which is closely related to amyloid-β (Aβ) generation, abnormal tau phosphorylation, oxidative stress, and apoptosis. Alterations in membranal components, including cholesterol and fatty acids, their characteristics, disposition, and distribution along the membranes, have been studied as evidence of cell membrane alterations in AD brain. The majority of these studies have been focused on the cytoplasmic membrane; meanwhile the mitochondrial membranes have been less explored. In this work, we studied lipids and mitochondrial membranes in vivo, following intracerebral injection of fibrillar amyloid-β (Aβ). The purpose was to determine how Aβ may be responsible for beginning of a vicious cycle where oxidative stress and alterations in cholesterol, lipids and fatty acids, feed back on each other to cause mitochondrial dysfunction. We observed changes in mitochondrial membrane lipids, and fatty acids, following intracerebral injection of fibrillar Aβ in aged Wistar rats. Melatonin, a well-known antioxidant and neuroimmunomodulator indoleamine, reversed some of these alterations and protected mitochondrial membranes from obvious damage. Additionally, melatonin increased the levels of linolenic and n-3 eicosapentaenoic acid, in the same site where amyloid β was injected, favoring an endogenous anti-inflammatory pathway

Accumulation of Exogenous Amyloid-Beta Peptide in Hippocampal Mitochondria Causes Their Dysfunction: A Protective Role for Melatonin

Amyloid-beta (Aβ) pathology is related to mitochondrial dysfunction accompanied by energy reduction and an elevated production of reactive oxygen species (ROS). Monomers and oligomers of Aβ have been found inside mitochondria where they accumulate in a time-dependent manner as demonstrated in transgenic mice and in Alzheimer's disease (AD) brain. We hypothesize that the internalization of extracellular Aβ aggregates is the major cause of mitochondrial damage and here we report that following the injection of fibrillar Aβ into the hippocampus, there is severe axonal damage which is accompanied by the entrance of Aβ into the cell. Thereafter, Aβ appears in mitochondria where it is linked to alterations in the ionic gradient across the inner mitochondrial membrane. This effect is accompanied by disruption of subcellular structure, oxidative stress, and a significant reduction in both the respiratory control ratio and in the hydrolytic activity of ATPase. Orally administrated melatonin reduced oxidative stress, improved the mitochondrial respiratory control ratio, and ameliorated the energy imbalance

Melatonin Mitigates Mitochondrial Meltdown: Interactions with SIRT3

Melatonin exhibits extraordinary diversity in terms of its functions and distribution. When discovered, it was thought to be uniquely of pineal gland origin. Subsequently, melatonin synthesis was identified in a variety of organs and recently it was shown to be produced in the mitochondria. Since mitochondria exist in every cell, with a few exceptions, it means that every vertebrate, invertebrate, and plant cell producesmelatonin. The mitochondrial synthesis ofmelatonin is not photoperiod-dependent, but itmay be inducible under conditions of stress. Mitochondria-produced melatonin is not released into the systemic circulation, but rather is used primarily in its cell of origin. Melatonin’s functions in the mitochondria are highly diverse, not unlike those of sirtuin 3 (SIRT3). SIRT3 is an NAD+-dependent deacetylase which regulates, among many functions, the redox state of the mitochondria. Recent data proves that melatonin and SIRT3 post-translationally collaborate in regulating free radical generation and removal from mitochondria. Since melatonin and SIRT3 have cohabitated in the mitochondria for many eons, we predict that these molecules interact in many other ways to control mitochondrial physiology. It is predicted that these mutual functions will be intensely investigated in the next decade and importantly, we assume that the findings will have significant applications for preventing/delaying some age-related diseases and aging itself