Effect of α-Ketoglutarate on Cyanide-induced Biochemical Alterations in Rat Brain and Liver

Objective To investigate the biochemical changes in rat brain and liver following acute exposure to a lethal dose of cyanide, and its response to treatment of α-ketoglutarate （α-KG） in the absence or presence of sodium thiosulfate （STS）. Methods Female rats were administered 2.0 LD50 potassium cyanide （KCN; oral） in the absence or presence of pre-treatment （-10 rain）, simultaneous treatment （0 rain） or post-treatment （＋2-3 min） of α-KG （2.0 g/kg, oral） and/or STS （1.0 g/kg, intraperitoneal, -15 min, 0 rain or ＋ 2-3 min）. At the time of onset of signs and symptoms of KCN toxicity （2-4 min） and at the time of death （5-15 min）, various parameters particularly akin to oxidative stress viz. cytochrome oxidase （CYTOX）, superoxide dismutase （SOD）, glutathione peroxidase （GPx）, reduced glutathione （GSH） and oxidized glutathione （GSSG） in brain, and CYTOX, sorbitol dehydrogenase （SDH）, alkaline phosphatase （ALP）, GSH and GSSG in liver homogenate were measured. Results At both time intervals brain CYTOX, SOD, GPx, and GSH significantly reduced （percent inhibition compared to control） to 24%, 56%, 77%, and 65%, and 44%, 46%, 78%, and 57%, respectively. At the corresponding time points liver CYTOX and GSH reduced to 74% and 63%, and 44% and 68%, respectively. The levels of GSSG in the brain and liver, and hepatic ALP and SDH were unchanged, Pre-treatment and simultaneous treatment of α-KG alone or with STS conferred significant protection on above variables. Post-treatment was effective in restoring the changes in liver but failed to normalize the changes in the brain. Conclusions Oral treatment with α-KG alone or in combination with STS has protective effects on cyanide-induced biochemical alterations in rat brain and liver.

Equilibrium and kinetics of adsorption of Ca(Ⅱ) ions onto KCTS and HKCTS

The adsorption of Ca（ II ） ions from aqueous solution by ehitosan a-ketoglutaric acid （KCTS） and hydroxamated chitosan a-ketoglutaric acid （HKCTS） was studied in a batch adsorption system. The Langmuir and Freundlich adsorption models were applied to describing the equilibrium isotherms, and isotherm constants were determined. The kinetics of the adsorption with respect to the initial Ca（II） ions concentration, temperature and pH was investigated. The pseudo-first-order and second-order kinetic models were used to describe the kinetic data and the rate constants were evaluated. The results show that the experimental data fit well to the Langmuir isotherms with a high correlation coefficient （R2）. The pseudo-second-order rate expression provides the best fitting kinetic model. The pseudo second-order kinetic model is indicated with the activation energy of 26.22 kJ/mol and 6.16 kJ/mol for KCTS and HKCTS, respectively. It is suggested that the overall rate of adsorption of Ca（ II ） ions is likely to be controlled by the chemical process.

Analysis of isocitrate dehydrogenase-1/2 gene mutations in gliomas

Objective To highlight recent researches which may show promise for histomolecular classification and new treatments for gliomas.Data sources All articles cited in this review were mainly searched from PubMed, which were published in English from 1996 to 2010.Study selection Original articles and critical reviews selected were relevant to the isocitrate dehydrogenase-1/2 mutation in gliomas and other tumors.Results Extraordinary high rates of somatic mutations in isocitrate dehydrogenase-1/2 occur in the majority of World Health Organization grade Ⅱ and grade Ⅲ gliomas as well as grade Ⅳ secondary glioblastomas. Isocitrate dehydrogenase-1/2 mutations are associated with younger age at diagnosis and a better prognosis in patients with mutated tumors. The functional role of isocitrate dehydrogenase-1/2 mutations in the pathogenesis of gliomas is still unclear.Conclusion Isocitrate dehydrogenase-1/2 mutations define a specific subtype of gliomas and may have great significance in the diagnosis, prognosis, and treatment of patients with these tumors.