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.