Grape seed procyanidin supplementation to rats fed a high-fat diet during pregnancy and lactation increases the body fat content and modulates the inflammatory response and the adipose tissue metabolism of the male offspring in youth.

OBJECTIVE: Procyanidins are polyphenolic bioactive compounds that exert beneficial effects against obesity and its related diseases. The aim of this study was to evaluate whether supplementation with low doses of a grape seed procyanidin extract (GSPE) to rats during pre- and postnatal periods provides biological effects to their offspring in youth. DESIGN: The metabolic programming effect of GSPE was evaluated in the 30-day-old male offspring of four groups of rats that were fed either a standard diet (STD) or a high-fat diet (HFD) and that were supplemented with either GSPE (25 mg kg(-1) of body weight per day) or vehicle during pregnancy and lactation. RESULTS: Significant increases in the adiposity index and in the weights of all the white adipose tissue depots studied (retroperitoneal, mesenteric, epididymal (EWAT) and inguinal) were observed in the offspring of rats that were fed a HFD and that were treated with GSPE (HFD-GSPE group) compared with the offspring of rats that were fed the same diet but that did not receive the procyanidins (HFD group). The HFD-GSPE animals also exhibited a higher number of cells in the EWAT, a sharp decrease in the circulating levels of monocyte chemoattractant protein-1 (MCP-1) and a moderate decrease in the plasma glycerol levels. The transcriptomic analysis performed in the EWAT showed 238 genes that were differentially expressed between the HFD and the HFD-GSPE animals, most of which were associated with the immune function and the inflammatory response, in addition to genes associated with adipose tissue remodeling and function, lipid and glucose homeostasis and the metabolism of methyl groups. CONCLUSION: The GSPE treatment in rats that were fed an HFD during pregnancy and lactation induced a clear metabolic programming effect in the offspring, increasing adiposity, decreasing the circulating levels of MCP-1 and changing the gene expression in the EWAT toward a better inflammatory profile.

Mitochondrial injury in human acute carbon monoxide poisoning: the effect of oxygen treatment.

The best oxygen therapy for acute carbon monoxide poisoning (ACOP) remains unestablished. Reported mitochondrial complex IV (mtCIV) inhibition, together with carboxyhaemoglobin (COHb)-induced hypoxia, may influence acute clinical symptoms and outcome. To "mitochondrially" evaluate treatment efficacy, we correlated intoxication severity and symptoms with mitochondrial function (mtCIV activity) and oxidative stress (lipid peroxidation) in 60 poisoned patients and determined ACOP recovery depending on either normobaric or hyperbaric oxygen therapy along a 3-month follow-up. In the present article we positively evaluate mtCIV as a good marker of ACOP recovery, treatment effectiveness, and late neurological syndrome development, which advocates for hyperbaric oxygen therapy as the treatment of choice. However, we discourage its usefulness as a severity marker because of its excessive sensitivity. We additionally evaluate oxidative stress role and prognostic factors for neurological sequelae development.

Respiratory rate and quality changes in fresh-cut pears as affected by superatmospheric oxygen.

Changes in the respiration rate of fresh-cut "Flor de Invierno" pears stored under superatmospheric oxygen concentrations were studied and compared to those observed under traditional modified atmosphere packaging conditions. Changes in package headspace O(2) and CO(2) concentrations throughout storage were curve-fitted to nonlinear equations, calculating respiration rates by combining the derivatives of the equations and the gas permeations throughout storage. Moreover, relationships between respiratory activity and quality parameters of fresh-cut Flor de Invierno pears dipped into an antioxidant solution (0.75% N-acetylcysteine and 0.75% glutathione) were assessed. CO(2) production of fresh-cut Flor de Invierno pears stored under 70 kPa O(2) atmospheres was successfully estimated with the proposed mathematical procedure. This method also proved to describe well CO(2) production rates of fresh-cut pears stored under initial 2.5 kPa O(2)+ 7 kPa CO(2) or 21 kPa O(2). In addition, a modification of Michaelis-Menten enzyme kinetics was adequate to describe the changes in estimated CO(2) production due to fermentative processes occurring under low oxygen concentrations. Superatmospheric O(2) concentrations seem to promote oxidative processes, which result into a dramatical modification of some quality attributes of fresh-cut pears.

Intoxicación por monóxido de carbono: claves fisiopatológicas para un buen tratamiento / Carbon monoxide poisoning: pathophysiologic principles underlying good treatment

En España, la intoxicación por monóxido de carbono (ICO) es la intoxicación por gases más frecuente. Su causa más habitual son los accidentes domésticos debidos a la combustión incompleta de gases en estufas, calentadores, calderas, braseros y otros, así como la inhalación del humo de los incendios donde la ICO, junto al cianuro, constituyen la principal causa de víctimas mortales. La capacidad tóxica del monóxido de carbono(CO) depende, esencialmente, de su unión a dos moléculas que contienen el grupo heme: la hemoglobina, que como resultado causa hipoxia anóxica y la mayor parte de la sintomatología aguda, y los citocromos de la cadena respiratoria mitocondrial, con el consiguiente bloqueo de la respiración celular y a la que se atribuye la sintomatología diferida que se produce en algunos pacientes. Los signos y síntomas más frecuentes son cefalea (96,9%), mareo (66,1%), náuseas (35,8%), inestabilidad a la marcha(32%), pérdida de conciencia (29,2%) y taquicardia (20%). Los niños, embarazadas, ancianos y pacientes con coronariopatía previa se consideran población de riesgo de afectación severa. La confirmación diagnóstica es analítica: determinación sanguínea dela hemoglobina ocupada por CO mediante una analítica o con un pulsioxímetro y/o la detección de CO en aire espirado. Ante la sospecha de ICO, se debe evitar la entrada de más CO en el organismo, y retirar a la víctima de la fuente de inhalación, con autoprotección del personal de rescate, asistencia y ventilación del local. Debe administrarse de inmediato oxígeno en condiciones normobáricas a la mayor concentración posible (mascarilla de alto flujo o al 100% si está intubado) ante cualquier diagnóstico de sospecha, sin esperar la confirmación analítica. Se discute en esta revisión el uso de oxígeno hiperbárico en la ICO (AU)

Carbon monoxide (CO) poisoning is the most common form of gas poisoning in Spain. Most cases are household accidents due to incomplete combustion of gases by room heaters, water heaters, braziers and similar devices, or the result of smoke inhalation, where CO and cyanide poisoning account for most deaths. CO toxicity is a result of its binding to 2 heme molecules. Binding to hemoglobin causes hypoxia, anoxia, and the majority of acute symptoms. Binding to cytochromes in the mitochondrial respiratory chain leads to consequent inhibition of respiration at the cellular level, contributing to the differential signs and symptoms seen in some patients. The most frequent are headache (96.9%), nausea (66.1%), vomiting (35.8%), unstable gait (32%), loss of consciousness (29.2%), and tachycardia(20%). Children, pregnant women, the elderly, and individuals with a history of heart disease are at risk of severe poisoning. A diagnosis is confirmed by a blood test or pulse oximetry result indicating that CO is bound to hemoglobin or by the detection of CO in expired air. If CO poisoning is suspected, further exposure must be prevented by removing the victim from the source of inhalation, while also protecting rescuers and medical caregivers, and by ventilating the premises. Oxygen should be administered immediately at a normal pressure and at the highest concentration possible(through a high-flow mask or at 100% if the patient is intubated) even before laboratory findings confirm the diagnosis. This review includes a discussion of the use of hyperbaric oxygen to treat CO poisoning (AU)