Ponzoni Silvia
Departamento de Ciências Fisiológicas, Universidade Estadual de Londrina, Rodovia Celso Garcia Cid, PR 445, km 380, Campus Universitário, Londrina, PR, 86055-990, Brazil.
Invert Neurosci. 2017 Jun;17(2):5. doi: 10.1007/s10158-017-0198-7. Epub 2017 Apr 27.
Manganese (Mn) is an essential metal for the development and function of the mammalian brain; however, excess Mn accumulation may cause neurological abnormalities resembling Parkinson's disease due to reductions in brain dopamine levels. Because dopamine also regulates many functions in crustaceans, this study examined the effects of Mn accumulation in Dilocarcinus pagei, a Neotropical freshwater crab. Following a 72-h exposure to graded concentrations of MnCl, Mn accumulation was assessed in several tissues. Glycaemia and the tyrosine hydroxylase (TH) immunostaining response were also examined as indicators of catecholaminergic function and catecholaminergic cell integrity, respectively. Tissue Mn accumulation was variable and occurred in the following order: gills > hepatopancreas > claw muscle > haemolymph. Exposure to 2 mM Mn reduced the gill levels of calcium, copper and iron, whereas Mn at all concentrations decreased zinc levels. All Mn-exposed animals showed lower copper levels in the hepatopancreas and haemolymph. Exposure to 2.0 mM Mn increased the haemolymph calcium. Mn exposure had no effect on glycaemia, whereas exposure to low Mn concentrations reduced the TH immunostaining response. Analysis of the central nervous system revealed the greatest Mn effect in the cerebral ganglion and the least effect in the abdominal ganglia. These results suggest the operation of an adaptive mechanism for tissue accumulation that could be responsible for the lack of an association between Mn concentrations and metal accumulation. The findings also suggest that Mn, calcium, iron and zinc share a transporter in gill cells and that Mn resistance is greater in the TH-positive cells of this crustacean than in mammalian cells.
锰(Mn)是哺乳动物大脑发育和功能所必需的金属;然而,由于脑多巴胺水平降低,过量的锰积累可能会导致类似帕金森病的神经异常。由于多巴胺也调节甲壳类动物的许多功能,本研究考察了新热带淡水蟹——帕氏双角溪蟹(Dilocarcinus pagei)体内锰积累的影响。在暴露于分级浓度的氯化锰72小时后,评估了几个组织中的锰积累情况。还分别检测了血糖和酪氨酸羟化酶(TH)免疫染色反应,作为儿茶酚胺能功能和儿茶酚胺能细胞完整性的指标。组织中的锰积累情况各不相同,顺序如下:鳃>肝胰腺>爪肌>血淋巴。暴露于2 mM的锰会降低鳃中钙、铜和铁的水平,而所有浓度的锰都会降低锌的水平。所有暴露于锰的动物肝胰腺和血淋巴中的铜水平都较低。暴露于2.0 mM的锰会使血淋巴中的钙增加。锰暴露对血糖没有影响,而暴露于低浓度的锰会降低TH免疫染色反应。对中枢神经系统的分析显示,锰对脑神经节的影响最大,对腹神经节的影响最小。这些结果表明存在一种组织积累的适应性机制,这可能是锰浓度与金属积累之间缺乏关联的原因。研究结果还表明,锰、钙、铁和锌在鳃细胞中共享一个转运体,并且这种甲壳类动物的TH阳性细胞对锰的抗性比哺乳动物细胞更强。