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Two novel glycoside hydrolases were cloned from the genomic DNA of alklinphilic bacterium Cellulomonas bogoriensis 69B4 T and functionally expressed in Escherichia coli. The two enzymes shared less than 73% of identities with other known glycosidases and belonged to glycoside hydrolase families 5 and 9. Recombinant Cel5A exhibited optimum activity at pH 5.0 and at a temperature of 70 °C, and Cel9A showed optimum activity at pH 7.0 and at a temperature of 60 °C. The two enzymes exhibited activity at alkaline pH 11 and were stable over a wide range of pH. The maximum activities of Cel5A and Cel9A were observed in 0.5 M NaCl and 1 M KCl, respectively. In addition, these two enzymes exhibited excellent halostability with residual activities of more than 70% after pre-incubation for 6 days in 5 M NaCl or 4 M KCl. Substrate specificity analysis revealed that Cel5A and Cel9A specifically cleaved the β-1,4-glycosidic linkage in cellulose with the highest activity on carboxymethyl cellulose sodium (78.3 and 145.3 U/mg, respectively). Cel5A is an endoglucanase, whereas Cel9A exhibits endo and exo activities. As alkali-activated, thermo-tolerant, and salt-tolerant cellulases, Cel5A and Cel9A are promising candidates for further research and industrial applications.

Abstract. To investigate the Manganese(Mn)-induced toxicity on crucial oxidative damage parameters on brain of birds, 50-day-old male Hyline cocks were fed either a commercial diet or a Mn-supplemented diet. The following were determined: restraining ability to OH·, the activities of Na+-K+-ATPase, Mg 2+ -ATPase and Ca 2+ -ATPase, the activities of succinate dehydrogenase (SDH) and Calcineurin (CaN); Exposure to Mn significantly lowered restraining ability to OH·, the activities of ATP enzymes, activities of SDH and CaN. These findings suggested that Mn exposure resulted in the oxidative damage of cock cerebral tissue.

Abstract. Manganese (Mn) is known to be essential for maintaining the proper function and regulation of many biochemical. To investigate the toxicity of Mn on bird brains, 50-day-old cocks were fed either a commercial diet or a Mn-supplemented diet. the following were determined: Mn concentration, Ca2+ concentration, the expression of Calmodulin (CaM) and Calcineurin (CaN) gene. Exposure to Mn significantly lowered expression of CaM and CaN gene. However, Mn was accumulated in brain and the Ca2+ concentration was increased. These findings suggested that Mn exposure resulted in the damage of cock cerebral tissue by altering calcium homeostasis, which are possible underlying neurotoxicity mechanisms.