BACKGROUND & AIMS:
:Manganese (Mn) is a trace element known to be essential for maintaining the proper function and regulation of many biochemical and cellular reactions. However, little is known about the reproductive toxicity of Mn in birds. To investigate the toxicity of Mn on male reproduction in birds, 50-day-old cocks were fed either a commercial diet or a Mn-supplemented diet containing 600, 900, and 1800 mg/kg MnCl₂. After being treated with Mn for 30, 60, and 90 d, the following were determined: Mn content; histological and ultrastructural changes in the testes, apoptosis; the malondialdehyde (MDA) level; the activities of superoxide dismutase (SOD); the inhibition ability of hydroxyl radicals (OH); the levels of nitric oxide (NO), nitric oxide synthase (NOS), and protein carbonyl in the testes; the DNA-protein crosslinks (DPC); and the activity of the ATP enzyme. Exposure to Mn significantly lowered the activity of SOD and glutathione peroxidase (GPx) and the inhibition ability of OH. Mn exposure also increased the levels of MDA, NO, NOS, DPC, and protein carbonyl; the number of apoptotic cells; and the Mn content and caused obvious histopathological changes in the testes. These findings suggested that Mn exposure resulted in the oxidative damage of cock testicular tissue by altering radical formation, ATP enzyme systems, apoptosis, and DNA damage, which are possible underlying reproductive toxicity mechanisms induced by Mn exposure.
背景与目标:
: 锰 (Mn) 是一种微量元素,已知对维持许多生化和细胞反应的正常功能和调节至关重要。然而,对Mn在鸟类中的生殖毒性知之甚少。为了研究Mn对鸟类雄性繁殖的毒性,对50天大的公鸡进行了商业饮食或含有600,900和1800 mg/kg mncl 2的补充Mn的饮食。用Mn处理30、60和90 d后,测定以下含量: Mn含量; 睾丸的组织学和超微结构变化,细胞凋亡; 丙二醛 (MDA) 水平; 超氧化物歧化酶 (SOD) 的活性; 羟基自由基 (OH) 的抑制能力; 睾丸中一氧化氮 (NO),一氧化氮合酶 (NOS) 和蛋白羰基的水平; DNA-蛋白质交联 (DPC); 和ATP酶的活性。暴露于Mn会显着降低SOD和谷胱甘肽过氧化物酶 (GPx) 的活性以及OH的抑制能力。Mn暴露还增加了MDA,NO,NOS,DPC和羰基蛋白的水平; 凋亡细胞的数量; 和Mn含量,并在睾丸中引起明显的组织病理学变化。这些发现表明,Mn暴露通过改变自由基形成,ATP酶系统,凋亡和DNA损伤而导致公鸡睾丸组织的氧化损伤,这可能是Mn暴露引起的潜在生殖毒性机制。