Quantification of ruminal microbiota and production of methane and carbonic dioxide from diets with inclusion of glycerin / Quantificação da microbiota ruminal e produção de metano e gás carbônico de dietas com inclusão de glicerina

The aim of this study was to quantify the liquid-associated bacteria and protozoa of the rumen and to evaluate the potential of in vitro production of gases CH4 and CO2 of diets with inclusion of glycerin for sheep. Two diets were formulated with a roughage:concentrate ratio of 20:80, according to the presence or absence of glycerin: G0 - control, without glycerin; and G10 - 10% glycerin as part of the concentrate. To quantify the liquid-associated bacteria and protozoa from the rumen and production of CH4 and CO2 gases, a completely randomized design was used. The diets had no effect (P>0.05) on production and composition of liquid-associated protozoa and bacteria from the rumen of lambs. Likewise, a (P>0.05) diet effect was not observed on production of CH4 and CO2 in vitro, which presented average concentrations of 24.55mL/g MS and 51.52mL/g MS, respectively. The use of 10% glycerin did not alter production or composition of ruminal microflora, and moreover, did not negatively impact the production of CH4 and CO2 gases in vitro.

Objetivou-se com este estudo quantificar as bactérias e protozoários líquido-associados do rúmen e avaliar o potencial de produção dos gases CH4 e CO2 in vitro de dietas com inclusão de glicerina para ovinos. Duas dietas foram formuladas, na proporção volumoso:concentrado de 20:80, conforme a presença ou ausência de glicerina: G0 - controle sem glicerina, G10 - 10% glicerina como parte do concentrado. Para a quantificação das bactérias e protozoários líquido-associados do rúmen e produção dos gases CH4 e CO2, utilizou-se o delineamento inteiramente ao acaso. Não foi observado efeito de dieta (P>0,05) sobre a produção e composição de protozoários e bactérias líquido-associados do rúmen de cordeiros. Da mesma forma, não houve efeito de dieta (P>0,05) sobre a produção de CH4 e CO2 in vitro, os quais apresentaram concentrações médias de 24,55mL/g MS e 51,52mL/g MS, respectivamente. O uso de 10% glicerina não altera a produção ou composição da microflora ruminal, e também não impacta negativamente a produção dos gases CH4 e CO2 in vitro.

Halomethane-chlordecone (CD) interactive hepatotoxicity--current concepts on the mechanism.

Why is a low dose of toxic chemical nontoxic? What makes a larger dose of the same chemical toxic? Extensive work done to understand the mechanism of halomethane hepatotoxicity and its potentiation by chlorinated insecticide, chlordecone has resulted in the understanding of these basic tenets of toxicology. Studies suggest that ordinarily a small dose of halomethane causes limited liver injury which is accompanied by stimulated tissue repair enabling complete recovery from injury before manifestation. A large dose of halomethane becomes toxic due to suppressed tissue repair, which permits injury to progress in an unchecked fashion. Exposure to very low levels of chlordecone results in highly exaggerated toxicity of ordinarily nontoxic doses of halomethane because of suppressed hepatocellular regeneration and restoration, permitting the progression of liver injury ultimately resulting in liver failure and animal mortality. This concept is further supported by the observation that, while exposure to even high levels of phenobarbital and subsequent low nontoxic doses of halomethane results in greater level of initial liver injury, tissue repair is not completely suppressed; it is slightly postponed by 24 hr, but then much higher rate of tissue repair ensures and consequently enables the animals to completely recover from liver injury and survive. Thus, whether initiation of tissue repair processes occurs or not is the critical determinant in the ultimate manifestation of hepatotoxicity and its end result of either animal death or recovery and survival. Currently understood 'Mechanisms of toxicity' adequately explain only how toxic injury begins. These mechanisms do not permit us to predict the ultimate outcome of toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Site-site heterogeneity in isocitrate lyase of castor seed endosperm: evidence from kinetics of inactivation by tetranitromethane.

Inactivation of isocitrate lyase (native and EDTA-dialysed) by excess tetranitromethane (TNM) exhibits, biphasic kinetics, in which half of the initial activity is lost in a fast and the remaining half in a slow phase each following the pseudo-first order kinetics. Rate constants of the two phases are proportional to the TNM concentration. High succinate concentration protects the enzyme against TNM inactivation only in the slow phase without any effect on the fast phase. With the EDTA-dialysed enzyme, no such protection (against inactivation by TNM) is observed in the presence of succinate or Mg2+ ions. Addition of both these ligands together brings about protection against the slow phase (as with the native enzyme). It has been proposed that the site-site heterogeneity of isocitrate lyase is a consequence of its quaternary structure constraints.

Modificaciones del estado ácido-base del líquido cefalorraquídeo por efecto de la administración de alcalinizantes (bicarbonato de sodio y THAM) / Changes of the acid-base equilibrium of the cerebrospinal fluid by effect of administration of alkaline agents (sodium bicarbonate and THAM)

Cuando se infunde bicarbonato de sodio intravenoso el propósito de corregir la acidosis metabólica se obtienen resultados opuestos en el líquido cefalorraquídeo. La caída del pH en el líquido y, por lo tanto, en el sistema nervioso central, puede ocasionar empeoramiento en el estado de conciencia, modificación de la ventilación y modificación de la perfusión cerebral. Por el contrario, la infusión de THAM - Tris(hidroximetil)aminometano-, modifica en el mismo sentido el estado ácido-base en sangre, líquido cefalorraquídeo y, por lo tanto, en sistema nervioso central, logrando el objetivo de corregir la acidosis, sin introducir secuelas neurológicas. Para demostrar lo expuesto anteriormente, se trabajó con dos grupos de perros que fueron anestesiados y ventilados mecánicamente. A un grupo se le infundió bicarbonato de sodio intravenoso y al otro THAM por la misma vía. Se midieron los siguientes parámetros ácido-base en sangre arterial, venosa y líquido cefalorraquídeo; pH, presión parcial de dióxido de carbono, bicarbonato real, exceso de bases y THAM en el líquido, con un método que desarrollamos para tal fin