Malecki E A, Lo H C, Yang H, Davis C D, Ney D M, Greger J L
Department of Nutritional Sciences, University of Wisconsin-Madison 53706, USA.
JPEN J Parenter Enteral Nutr. 1995 May-Jun;19(3):222-6. doi: 10.1177/0148607195019003222.
Manganese is an essential but potentially toxic mineral. Parenteral administration of manganese via total parenteral nutrition (TPN) bypasses homeostatic mechanisms (intestinal absorption and presystemic hepatic elimination). Our objective in this study was to determine the effect of supplemental manganese in TPN solutions on manganese status in a rat model.
Male Sprague-Dawley rats underwent jugular catheterization and were given 61.0 +/- 0.4 g/d TPN solution providing 0.5 +/- 0.2 nmol manganese/g (Mn-; n = 6) or 16 +/- 3 nmol manganese/g (Mn+; n = 7) for 7 days. Reference rats (RF; n = 8) were fed a purified diet containing 1.3 mmol manganese/g.
Liver manganese decreased in both TPN groups, but tibia, spleen, and pancreas manganese concentrations were greater in Mn+ rats than in Mn- or RF rats. Although no treatment differences were seen in heart or liver manganese superoxide dismutase activity, heart copper-zinc superoxide dismutase activity was lower in the Mn+ rats than in Mn- or RF rats (p < .05). Glutathione peroxidase activity was depressed in livers of both Mn- and Mn+ rats relative to RF rats (p < .0001), which was not due to selenium deficiency.
Supplemental parenteral manganese is taken up to a greater extent by peripheral tissues than the liver. In this first report of antioxidant enzyme activities in animals maintained with TPN, we found that TPN as well as supplemental manganese can influence antioxidant enzyme activities. We conclude that it is generally unnecessary and potentially toxic to supplement TPN solutions with manganese during short-term usage.
锰是一种必需但具有潜在毒性的矿物质。通过全胃肠外营养(TPN)进行肠外锰给药绕过了体内稳态机制(肠道吸收和肝前消除)。我们在本研究中的目的是确定TPN溶液中补充锰对大鼠模型锰状态的影响。
雄性Sprague-Dawley大鼠进行颈静脉插管,并给予61.0±0.4 g/d的TPN溶液,其中锰含量为0.5±0.2 nmol/g(Mn-;n = 6)或16±3 nmol/g(Mn+;n = 7),持续7天。对照大鼠(RF;n = 8)喂食含1.3 mmol锰/g的纯化饮食。
两个TPN组的肝脏锰含量均下降,但Mn+组大鼠的胫骨、脾脏和胰腺锰浓度高于Mn-组或RF组大鼠。尽管在心脏或肝脏锰超氧化物歧化酶活性方面未观察到治疗差异,但Mn+组大鼠的心脏铜锌超氧化物歧化酶活性低于Mn-组或RF组大鼠(p < 0.05)。相对于RF组大鼠,Mn-组和Mn+组大鼠肝脏中的谷胱甘肽过氧化物酶活性均降低(p < 0.0001),这并非由于硒缺乏所致。
肠外补充的锰被外周组织摄取的程度高于肝脏。在这份关于用TPN维持的动物抗氧化酶活性的首次报告中,我们发现TPN以及补充的锰均可影响抗氧化酶活性。我们得出结论,在短期使用期间,通常没有必要在TPN溶液中补充锰,而且补充锰可能具有毒性。