Malecki E A, Greger J L
Department of Nutritional Sciences, University of Wisconsin-Madison 53706, USA.
J Nutr. 1996 Jan;126(1):27-33. doi: 10.1093/jn/126.1.27.
We demonstrated previously that dietary manganese (Mn) deficiency depressed Mn concentrations in most tissues and consistently depressed Mn superoxide dismutase (MnSOD) levels in heart. To examine the functional consequences of these effects, we fed weanling male Sprague-Dawley rats (n = 12/diet) diets containing 20% (wt/wt) corn oil or 19% menhaden oil + 1% corn oil by weight and 0.75 or 82 mg Mn/kg diet for 2 mo (the fish oil mixture was supplemented with (+)-(mixed)-alpha-tocopherol to the level in corn oil). Heart and liver Mn concentrations in the Mn-deficient rats were 56% of those in Mn-adequate rats (P < 0.0001), confirming Mn deficiency. The Mn-deficient rats had more conjugated dienes in heart mitochondria than Mn-adequate rats (P < 0.001); rats fed fish oil had more conjugated dienes than those fed corn oil (P < 0.001). The MnSOD activity was inversely correlated with conjugated dienes (r = -0.71, P < 0.005), and Mn-deficient rats had 37% less MnSOD activity in the heart than did Mn-adequate rats (P < 0.0001). The dietary treatments did not affect heart microsomal conjugated diene formation, possibly because of compensation by copper-zinc (CuZn) SOD activity; CuZnSOD activities were 35% greater in the hearts of Mn-deficient animals (P < 0.01). Liver was less sensitive to Mn deficiency than was the heart as judged by MnSOD activity and conjugated diene formation. This work is the first to demonstrate that dietary Mn protects against in vivo oxidation of heart mitochondrial membranes.
我们之前证明,饮食中缺锰会降低大多数组织中的锰浓度,并持续降低心脏中的锰超氧化物歧化酶(MnSOD)水平。为了研究这些影响的功能后果,我们给断乳雄性斯普拉格-道利大鼠(每组12只)喂食含20%(重量/重量)玉米油或19%鲱鱼油+1%玉米油(按重量计)以及0.75或82毫克锰/千克饮食的饲料,持续2个月(向鱼油混合物中添加(+)-(混合)-α-生育酚至玉米油中的水平)。缺锰大鼠心脏和肝脏中的锰浓度是锰充足大鼠的56%(P<0.0001),证实了缺锰。缺锰大鼠心脏线粒体中的共轭二烯比锰充足大鼠更多(P<0.001);喂食鱼油的大鼠比喂食玉米油的大鼠有更多共轭二烯(P<0.001)。MnSOD活性与共轭二烯呈负相关(r=-0.71,P<0.005),缺锰大鼠心脏中的MnSOD活性比锰充足大鼠低37%(P<0.0001)。饮食处理不影响心脏微粒体共轭二烯的形成,可能是因为铜锌(CuZn)SOD活性起到了补偿作用;缺锰动物心脏中的CuZnSOD活性高35%(P<0.01)。从MnSOD活性和共轭二烯形成情况判断,肝脏对缺锰的敏感性低于心脏。这项工作首次证明饮食中的锰可防止心脏线粒体膜在体内发生氧化。