ABSTRACT
Resumen La vida y obra del literato Horacio Quiroga ha estado signada por venenos en varias oportunidades. Profundo conocedor de la selva misionera, plasmó en sus personajes el conocimiento de ponzoñas y venenos que poseía su flora y su fauna. En cuanto a su vida personal y la de sus familiares, el veneno estuvo presente hasta sus últimos días. Se describen en este trabajo tanto los venenos detallados en su obra como también el desenlace de su suicidio con cianuro de potasio.
Abstract The life and the work of the writer Horacio Quiroga has been marked by poisons and venoms on several occasions. Connoisseur of the flora and fauna of the Misiones jungle, he reflected in his characters the knowledge of poisons and venoms that he possessed. As for his personal life and that of his family, the poison was present until his last days. Both the poisons and venoms detailed in his work as well as the outcome of his suicide with potassium cyanide are detailed in this work.
Subject(s)
Literature, Modern , Viper VenomsABSTRACT
Antiaris africana belongs to the family Moraceae, it is commonly called “False Iroko” tree and one of the medicinal plants used in treatment of mental and nervous disorders in Nigeria. We have previously established the neuroprotective properties of crude extract of A. africana. The present study was thus designed to investigate the neuroprotective effect of different solvent fractions of A. africana against cyanide neurotoxicity in vitro. Cyanide induced a significant (P<0.01) inhibition of NADH succinate dehydrogenase, a key enzyme in mitochondria function as well as significant increase in oxidative stress as observed in the high level of malonedialdehyde (MDA), protein carbonyl (PC) and activity of monoamine oxidase (MAO) and decreased concentration of reduced glutathione (GSH) as compared to the control. Co-administration with different solvent fractions of A. africana (hexane fraction [HFA], dichloromethane fraction [DFA] and methanolic fraction [MFA]) significantly ameliorated the toxic effect of KCN as compared to the induced, untreated group (P<0.05). The results in this study showed that HFA (79.04% reversal of NSD inhibitory activity of KCN), DFA (63.68% and 72.6% activity against KCN induced LPO and PC respectively). However, MFA showed the best activity against GSH depletion caused by KCN (12.21%) and inhibition of MAO activity induced by KCN (94.63%). In conclusion, all the fractions possess neuroprotective activities at varying degrees against mitochondria damage by KCN. This result further substantiated the ethnomedicinal usage of A. africana and can provide novel compounds in the treatment of mitochondria-related neurodegenerative diseases.
ABSTRACT
BACKGROUND AND OBJECTIVES: Recent studies have shown that many kinds of K+ channels, including the muscarinic K+ channel (KACh), are activated in the ischemic heart. It is known that these channels can be modulated by phosphorylation. However, little is known about the function of the KACh in ischemic hearts. In this study, we examined whether the KACh channel is mediated by protein kinase C (PKC) activation in rat atrial myocytes under ischemic conditions. MATERIALS AND METHODS: Single atrial cells of adult rat heart were prepared by collagenase digestion. Channel activity of KACh was recorded by cell-attached configuration from single atrial cells under ischemic conditions, using a patch clamp technique. To simulate ischemia, adenosine or potassium cyanide (KCN) was applied to atrial myocytes, and Western blot was performed to specify PKC isoforms. RESULTS: Adenosine and KCN markedly increased KACh channel activity. The responses to adenosine and KCN were increased 3-fold at mean open time from that observed with control. Channel activity of KACh was blocked by pretreatment with PKC antagonists such as sphingosine, Go 6976, and rottlerin. PKC alpha and PKC betaI isoform levels were increased in the membrane fraction of ischemic heart, indicating that ischemic stress might trigger translocation of cytosolic PKC to the cell membrane. CONCLUSION: These results show that KACh channels are modulated by PKC activation under ischemic conditions induced by adenosine or KCN. Therefore, the channels can protect the heart from ischemic stress by increasing channel activity.
Subject(s)
Adult , Animals , Humans , Rats , Adenosine , Blotting, Western , Cell Membrane , Collagenases , Cytosol , Digestion , Heart , Ischemia , Membranes , Muscle Cells , Phosphorylation , Potassium Cyanide , Protein Isoforms , Protein Kinase C , Protein Kinases , SphingosineABSTRACT
Se estudió la estabilidad a largo plazo del juego de reactivos para la determinación de hemoglobina en sangre, basado en el comportamiento de la estabilidad física y química de los componentes del juego durante 1 año, así como también el ensayo funcional de éstos. Se estudió además el reactivo de trabajo durante 15 d. Un análisis estadístico de los resultados demostró que el juego de reactivos es estable durante los tiempos de estudio, almacenado a una temperatura de 2 a 8 EC.
The long term stability of the reagents kit to determine hemoglobin in blood, based on the physical and chemical stability of the components of the kit during a year, as well as their functional assay, were studied. The working resgent was also studied for 15 days. A statistical analysis of the results showed that the reagents kit is stable during the time under study, stored at a temperature from 2 to 8 EC.
ABSTRACT
Berberine sulfate ( Ber ) sc prolonged the survival time of mice under the condition of closed normobaric hypoxia, but Ber ig did not. Ber sc antagonized the effects of decreasing the survival time of mice by ip isoprenaline or phentolamine under the condition of closed normobaric hypoxia, prolonged decapitation-induced gasping duration in mice, and prolonged the survival time in mice poisoned by KCN, NaNO2 or lidocaine. Ber ig prolonged decapitation-induced gasping duration and the survival time in mice poisoned by lidocaine, too. But the effects of Ber ig were not so potent as Ber sc. The antianoxic effects of Ber was shown to be decreasing O2 consumption of body and raising the ability of body to utilize O2 under the condition of hypoxia.
ABSTRACT
in this paper we report the blood cobalt, methemoglobin and blood cyanide concentration-time equations and related parameters of pharmacokinetics after abministra-tion of sodium cobaltinitrite(18.6mg/kg)or potassium cyanide(3mg/kg)in dogs.It was found that 10% dimethyl sulfoxide used as a solvent, as compared with water, accelerated sodium cobaltinitrite absorption by intramuscular administration.The half absorption time was reduced from 14.5 min to 5.5 min, the time of maximum concentration of blood cobalt reduced from 1.11 h to 0.56 h, and the maximum conce-tration of blood cobalt raised from 2.71?g/ml to 3.35?g/ml.There was a significant difference of blood cobalt concentrasions between 10-60 and 120 min after intramuscular administration.