补充维生素B_1、B_2及C对大鼠脑功能的影响

用普通奶粉和强化维生素Ｂ１、Ｂ２及Ｃ的奶粉进行对比实验，观察补充维生素对大鼠脑功能的影响。补充维生素后大鼠行为功能测试表明：错误反应率和逃避时间均明显下降，海马乙酰胆碱神经递质明显增加，脑脂质过氧化物水平降低（Ｐ＜０．０５），而大鼠身体发育无明显改变。提示，在满足机体发育下适当补充维生素Ｂ１、Ｂ２和Ｃ可改善脑功能。     

甲基维生素B12拮抗甲基汞毒性的毒理学研究

甲基维生素Ｂ_（１２）拮抗甲基汞毒性的毒理学研究哈尔滨医科大学公共卫生学院（１５０００１）任莹，王蕊，李蓉，陈炳卿哈尔滨医科大学病理教研室李仁甲基汞不仅具有很强的神经毒而且对机体的免疫系统有明显的抑制作用［１］，本文从免疫毒理学角度探讨甲基维生素Ｂ１?..     

叶酸、维生素B_（12）与神经管缺陷

叶酸、维生素Ｂ１２是人体必须维生素，无论饮食摄入减少或／及代谢异常导致的叶酸、维生素Ｂ１２缺乏，均有可能引发胎儿神经管缺陷。孕前／孕期适当补充叶酸和维生素Ｂ１２可减少神经管缺陷的发病风险。     

城乡孕妇同型半胱氨酸代谢与神经管畸形的相关性研究

通过比较城乡早孕妇女血清同型半胱氨酸（Ｈｃｙ）、叶酸和维生素Ｂ１２水平，探讨Ｈｃｙ代谢与神经管畸形城乡差异的关系。随机抽取北京地区早孕妇女血清库中４１１份血清（城市１９５份，乡村２１６份），用高效液相色谱结合电化学方法检测血清中Ｈｃｙ浓度，放射免疫方法检测叶酸和维生素Ｂ１２浓度。结果：乡村孕妇Ｈｃｙ平均水平明显高于城市，分别为９．３１μｍｏｌ／Ｌ和５．７３μｍｏｌ／Ｌ；Ｂ１２水平则低于城市，分别为２１０．０９ｐｍｏｌ／Ｌ和２３３．３５ｐｍｏｌ／Ｌ，叶酸水平虽高于城市，但叶酸缺乏率的差异不显著。乡村孕妇的叶酸／Ｈｃｙ和Ｂ１２／Ｈｃｙ值均显著低于城市孕妇。提示Ｈｃｙ代谢异常与乡村神经管畸形高发有关。     

维生素B_6对硒的生物利用率影响的研究Ⅴ．大鼠硒利用率与维生素B_6剂量的依赖关系

４周龄雄性大鼠饲缺维生素Ｂ６（ＶＢ６）、缺硒的酪蛋白蔗糖基础饲料，３周后按体重分成４组，即：在基础饲料中补硒酸钠形式硒０．２５ｍｇ／ｋｇ和不同剂量的盐酸吡哆醇０，１．０，２．５和５．０ｍｌ／ｋｇ。实验期为４周，结果表明：体重增长、器官重量、ＶＢ６依存的胱硫醚酶活性、红细胞和骨骼肌中硒含量以及谷胱甘肽过化物酶活性对补ＶＢ６的反应最明显，以补ＶＢ６２．５ｍｇ／ｋｇ效果最佳。缺ＶＢ６时，仅补适量硒，组织中脂质过氧化物含量与缺硒缺ＶＢ６组无显著差别；而缺硒时仅补ＶＢ６２．５ｍｇ／ｋｇ即可显著降低脂质过氧化物含量。提示从维持组织中硒、ＧＳＨ－Ｐｘ活性以及降低脂质过氧化物水平方面，补ＶＢ６２．５ｍｇ／ｋｇ可以满足需要，ＶＢ６抗脂质过氧化物的作用与硒无关     

红细胞门冬氨酸转氨酶活性系数评价实验性维生素B_6缺乏

通过对小鼠Ｂ６不同含量的饲料（缺乏、充裕、普通）的喂养，证实了红细胞内门冬氨酸转氨酶（ＥＡＳＴ）的活性系数（ＡＣ）与小鼠维生素Ｂ６缺乏密切相关，当小鼠缺乏维生素Ｂ６一周时，ＡＣ值迅速提高。提出ＡＣ值＞１．８时，可认为是维生素Ｂ６缺乏。该法测定ＥＡＳＴ的ＡＣ值的变异系数为２．９３～３．８９％，方法简便，重现性好。     

婴幼儿边缘型维生素B_1缺乏症

目的探讨婴幼儿夜寐不安的原因及更有效地治疗夜寐不安的婴幼儿。方法对２５例以夜寐不安为主要表现，同时伴有烦躁、纳差的２岁以下小儿进行临床观察和红细胞转酮醇酶活力（ＴＰＰ效应）的测定。结果１６％的小儿属边缘型维生素Ｂ１缺乏，２０％属严重缺乏，而对照组小儿仅有６．７％属维生素Ｂ１缺乏症。经统计学处理，两组有显著差异（Ｐ＜０．０５）。实验组小儿经补充维生素Ｂ１１０ｍｇ１日３次口服１周后，临床症状明显好转的约占５０％，好转占３０％～４０％，而症状无改善的仅占１０％左右。治疗前ＴＰＰ效应异常者，经上述治疗后ＴＰＰ效应全部转为正常。结论口服补充维生素Ｂ１对治疗边缘型维生素Ｂ１缺乏症的效果是满意的。     

维生素B_6的离子交换HPLC法测定

本实验详细地研究了维生素Ｂ＿６（吡哆醛，ＰＬ；吡哆醇，ＰＮ；吡哆胺，ＰＭ）在阳离子交换树脂柱ＩＳＣ－０７／Ｓ１５０４上的色谱行为，建立了测定各种样品中维生素Ｂ＿６含量的高效液相色谱法。方法采用甲酸盐作流动相，荧光检测（Ｅｘ３２０ｎｍ，Ｅｍ４００ｎｍ）；对于不同的样品采取不同的提取、净化和分离方式。维生素Ｂ＿６组分与杂质之间以及维生素Ｂ＿６组分之间达到了基线分离。方法的标准添加回收率：８２．６％～１１１．３％，荧光响应值与标准量间的相关系数＞０．９９９，变异系数（ＣＶ）：０．４１％～０．６２％，最小检出量；ＰＬ，８．９７３×１０￣（－４）μｍｏｌ／Ｌ；ＰＮ，５．９１１×１０￣（－４）μｍｏｌ／Ｌ；ＰＭ，２．９７３×１０￣（－４）μｍｏｌ／Ｌ。     

孕妇维生素营养状况的研究

追踪调查了９００余名孕妇在妊娠早、晚期维生素Ａ、Ｅ、Ｂ１、Ｂ２及维生素Ｃ的摄入情况。并对其中４００余例孕妇孕中、晚期血清和新生儿脐血清维生素Ａ、Ｅ、Ｃ含量、全血谷胱甘肽还原酶活性系数（ＡＣ）、全血红细胞转酮醇酶效应值（ＴＰＰ％）进行了测定。结果发现维生素的摄入量于孕中期，除维生素Ａ和维生素Ｂ１分别为ＲＤＡ的６０％和６４．８％外，其余均达ＲＤＡ的８０％以上；孕晚期除维生素Ｂ１仍为ＲＤＡ的６４％外，其余均达ＲＤＡ的９０％以上。血液测定结果，维生素Ａ、Ｅ的量随孕期延续而上升，有９５％以上孕妇在参考标准范围以上。脐血中的维生素Ａ、Ｅ均比孕晚期含量低，分别为１１．２５±０．６２和（１２．６４±６．０４）μｍｏｌ／Ｌ；血清维生素Ｃ均超过８５μｍｏｌ／Ｌ，孕中、晚期和脐血含量分别为１２５．０３±３８．８１、１０７．９１±３５．７７和（１０５．４１±４３．９５）μｍｏｌ／Ｌ；ＡＣ值均低于１．３，孕中、晚期及脐血分别为１．１４±０．１５、１．１４±０．１２和１．１３±０．４３；ＴＰＰ值均高于２５％，孕中、晚期及脐血分别为３６．８２±３１．２１、２９．２９±２５．２８和（３８．５５±３８．２２）％。提示，孕妇维生素Ａ、Ｅ、Ｂ２?     

膳食维生素B_6对硒的生物利用率影响的研究 Ⅰ．对补硒大鼠组织硒含量的影响

研究膳食维生素Ｂ６（ＶＢ６）对大鼠组织中硒水平的影响。喂饲４周龄断乳雄性大鼠缺ＶＢ６缺硒的酪蛋白蔗糖基础膳食，２周后按体重把动物分成１０组。实验是２×２×２析因设计，２个水平ＶＢ６（每克膳食含０和２．５０μｇ盐酸吡哆醇），２种形式硒（亚硒酸钠和ＤＬ－硒蛋氨酸），２个硒水平（每公斤膳食含０．５和５．０ｍｇ硒），加上２个缺硒组（缺ＶＢ６和补ＶＢ６）。实验期为４周。结果在饲硒蛋氨酸的缺ＶＢ６组，血浆硒水平高于对应的补ＶＢ６组，但是缺ＶＢ６各组的红细胞中硒含量均显著低于补ＶＢ６各组。缺ＶＢ６时，饲亚硒酸钠动物的骨骼肌和心肌中硒水平均显著低于补ＶＢ６的动物；饲硒蛋氨酸大鼠的骨骼肌、心肌、脾、肝和肾脏中硒含量均显著高于补ＶＢ６组。提示ＶＢ６参与了硒在体内的转运以及硒蛋氨酸在肝脏中的代谢过程。     

Hypoxia-induced megaloblastosis in vitamin B12-deficient rats

In rats, in contrast with human subjects who develop megaloblastic anaemia due to vitamin B12 deficiency, haematological abnormalities with anaemia were not observed under normoxic conditions even though plasma vitamin B12 concentration was reduced to <15 % of a normal concentration by depleting dietary vitamin B12. To elucidate whether erythropoiesis was affected by vitamin B12 deficiency in rats, these vitamin B12-deficient rats were exposed to hypoxia (10.5 % O2) to stimulate erythropoiesis. In the vitamin B12-sufficient control rats, erythrocyte count was significantly (P<0.05) increased 1 week after starting the hypoxic exposure. However, the hypoxia-induced erythropoiesis was affected by vitamin B12 deficiency, and no significant increase in the erythrocyte count was observed even after 6-week exposure to hypoxia in the vitamin B12-deficient rats. In the vitamin B12-deficient rats in hypoxia, erythrocytes became abnormally enlarged, and haemoglobin concentration in peripheral blood was increased in proportion to the increase of mean corpuscular volume. However, the level of the increase in the haemoglobin concentration was significantly (P<0.05) lower in the vitamin B12-deficient rats compared with that in the -sufficient controls. In addition, in the vitamin B12-deficient rats, in contrast to the -sufficient rats, serum erythropoietin concentration was not normalized even after 6-week exposure to hypoxia. These results indicate that a megaloblastic anaemia-like symptom is induced when the vitamin B12-deficient rats are exposed to hypoxia.     

Effects of vitamin B12 deficiency on lipid metabolism of the rat liver and nervous system

1. Rats bred from vitamin B12-depleted dams were fed on a vitamin B12-deficient diet for 12-15 months and developed a severe vitamin B12 deficiency, as judged from methylmalonic acid excretion and tissue vitamin B12 levels at slaughter. Control rats were supplemented with vitamin B12 in the drinking-water. 2. Neurological signs were recorded after 7 months but the motor nerve conduction velocities remained normal. Neuropathological examination revealed mild changes in the peripheral nerves but no changes in the central nervous system. 3. The amounts of total lipids and phospholipids were normal, but in all examined tissues the proportions of pentadecanoate (C15 fatty acid) and heptadecanoate (C17 fatty acid) were considerably increased in vitamin B12 deficiency. 4. 3H2O was incorporated to the same extent into the fatty acids of nervous tissue from vitamin B12-deficient and control rats after 48 h. Less 3H was found in the liver fatty acids of the vitamin B12-deficient rats. 5. Neurological dysfunction can be demonstrated in the vitamin B12-deficient rat; the relation of the biochemical and neuropathological changes to the neurological signs needs further study.     

Effects of vitamin B12-deficiency on testes tissue in rats.

The state of vitamin B12-deficiency in rats was evaluated by determination of hepatic vitamin B12-dependent enzyme activities after the animals had fed on a vitamin B12-deficient soybean protein diet for 150 days. The effect of vitamin B12-deficiency on testicular tissue was also studied by morphological observations. Growth of vitamin B12-deficient rats was retarded and marked increase in urinary methylmalonic acid was observed. Vitamin B12 contents in the organs were depressed distinctly by the deficiency, especially in testes, vitamin B12 content decreased to 2.5 ng/g. Hepatic methionine synthase and methylmalonyl-CoA mutase activities showed striking depression to 5% of the control rats and extreme vitamin B12-deficiency was confirmed. Testes weight also showed marked decrease together with their relative weight per 100 g body weight. Morphological observations of testes of vitamin B12-deficient rats revealed atrophy of the seminiferous tubules and aplasia of sperms and spermatids. The above results proved that vitamin B12-deficiency affected rat testes, and suggested that the rat could be the animal model for elucidation of the mechanism of B12 action on testicular functions.     

Changes in CD4+CD8-/CD4-CD8+ ratio and humoral immune functions in vitamin B12-deficient rats

To clarify the role of vitamin B12 in the function of cell-mediated and humoral immune functions, the splenocytes expression of CD4, CD8 and serum C3, IgM, IgG concentrations were examined in vitamin B12-deficient rats, and the effect of the administration of methylcobalamin was also studied. The CD4+CD8-/CD4-CD8+ ratio in splenocytes was significantly higher in vitamin B12-deficient rats than in control rats (p < 0.05). The value in the 48 hours after methylcobalamin administration group, was within the normal range (p < 0.05). From these results, the elevation of the CD4+CD8-/CD4-CD8+ ratio by vitamin B12-deficiency was confirmed in rats. The serum C3, IgM and IgG concentrations were lower in the vitamin B12-deficient group than in the control group. These findings suggest that vitamin B12 plays a role in maintaining the immune function in rats.     

Lipid composition and metabolism in liver and brain of vitamin B12-deficient rat sucklings.

1. Rat sucklings (18-d-old) bred from vitamin B12-deprived dams were compared with vitamin B12-supplemented dams' offspring, which were considered normal rat sucklings. 2. The vitamin B12-deficient rat sucklings had lower body-weight, liver weight and brain weight. 3. Vitamin B12 deficiency was also evident from the tenfold lower concentrations of vitamin B12 in liver and cerebellum. 4. The concentration of liver lipid was markedly increased in vitamin B12-deficient rats; triacylglycerol accounted for most of the increase. In brain the lipid concentration was slightly decreased (less than 0.05). 5. The methylation of ethanolamine phosphoglyceride to choline phosphoglyceride was reduced in both liver and brain in vitamin B12-deficient rats, as measured after the administration of [14C]ethanolamine. A slight decrease in choline phosphoglyceride concentration could be a consequence of this finding. The composition of phospholipids was otherwise normal. 6. Odd-chain fatty acids (pentadecanoate and heptadecanoate) accumulated in both liver and brain of the vitamin B12-deficient rat sucklings and constituted approximately 1% of total fatty acid. 7. The biosynthesis of fatty acid and cholesterol from intraperitoneally-injected 3H2O and [14C]propionate was unchanged in vitamin B12 deficiency.     

Necessity of vitamin B12 for growth of rats fed on an odd- or even-carbon-number fat

1. The effect of vitamin B12 on growth was studied in young male and female rats fed on diets sufficient (+B12) or deficient (-B12) in vitamin B12 containing 30% of the dietary energy as fat, either maize oil (CO) or triundecanoin (TUD). 2. Vitamin B12 deficiency severely depressed growth. After 6 weeks the weight gain of CO(-B12) rats was only 72% of that of CO(+B12) rats and the gain of TUD(-B12) rats was only 47% of TUD(+B12) rats. 3. After fasting 24 or 96 h TUD-fed rats, both +B12 and -B12, had greater glycogen reserves and higher plasma glucose levels than CO-fed rats. 4. It is concluded that vitamin B12 is required for the metabolism and utilization of both an odd-carbon-number medium-chain fat, TUD, and an even-C-number long-chain fat, CO, during growth in rats.     

Feeding dried purple laver (nori) to vitamin B12-deficient rats significantly improves vitamin B12 status.

To clarify the bioavailability of vitamin B12 in lyophylized purple laver (nori; Porphyra yezoensis), total vitamin B12 and vitamin B12 analogue contents in the laver were determined, and the effects of feeding the laver to vitamin B12-deficient rats were investigated. The amount of total vitamin B12 in the dried purple laver was estimated to be 54.5 and 58.6 (se 5.3 and 7.5 respectively) microg/100 g dry weight by Lactobacillus bioassay and chemiluminescent assay with hog intrinsic factor respectively. The purple laver contained five types of biologically active vitamin B12 compounds (cyano-, hydroxo-, sulfito-, adenosyl- and methylcobalamin), in which the vitamin B12 coezymes (adenosyl- and methylcobalamin) comprised about 60 % of the total vitamin B12. When 9-week-old vitamin B12-deficient rats, which excreted substantial amounts of methylmalonic acid (71.7(se 20.2) micromol/d) in urine, were fed the diet supplemented with dried purple laver (10 microg/kg diet) for 20 d, urinary methylmalonic acid excretion (as an index of vitamin B12 deficiency) became undetectable and hepatic vitamin B12 (especially adenosylcobalamin) levels were significantly increased. These results indicate that vitamin B12 in dried purple laver is bioavailable to rats.     

Characterization and bioavailability of vitamin B12-compounds from edible algae

Substantial amounts of vitamin B12 were found in some edible algae (green and purple lavers) and algal health food (chlorella and spirulina tablets) using the Lactobacillus delbrueckii subsp. lactis ATCC7830 microbiological assay method. Corrinoid-compounds were purified and characterized from these algae to clarify the chemical properties and bioavailability of the algal vitamin B12. True vitamin B12 is the predominate cobamide of green and purple lavers and chlorella tablets. Feeding the purple laver to vitamin B12-deficient rats significantly improved the vitamin B12 status. The results suggest that algal vitamin B12 is a bioavailable source for mammals. Pseudovitamin B12 (an inactive corrinoid) predominated in the spirulina tablets, which are not suitable for use as a vitamin B12 source, especially for vegetarians. algal health food, bioavailability, cobalamin, edible algae, vitamin B12     

维生素B_(12)影响同型半胱氨酸对大鼠认知能力的作用

目的:观察同型半胱氨酸(homocysteine,Hcy)对大鼠空间认知能力的影响及维生素B12(VB12)的干预作用。方法:大鼠随机分为对照组,实验组及VB12干预组。测定各组血浆Hcy,血清VB12水平和Y迷宫学习记忆情况,并对大鼠海马区进行乙酰胆碱酯酶(acetylcholinesterase,AChE)免疫组化分析。结果:实验组血浆Hcy水平比对照组升高,并出现空间认知障碍,且两组差异有显著性;实验组海马区AChE阳性纤维减少,呈弱阳性(+)。VB12干预组血浆Hcy水平与对照组比无明显变化,但VB12升高,无空间认知障碍发生;VB12干预组海马区有大量的AChE纤维,呈强阳性(+++)。结论:高同型半胱氨酸可引起大鼠空间认知障碍,而VB12可降低Hcy水平并干预空间认知障碍的发生。     

The effects of dietary histidine, methionine and homocystine on vitamin B12 and folate levels in rat liver.

1. L-histidine (20 g/kg) added to vitamin B12-deficient and cyanocobalamin-supplemented diets based on soya-bean flour reduced the growth of rats given the vitamin B12-deficient diet but stimulated growth of rats given the cyanocobalamin-supplemented diet. Liver weight (g/kg body-weight)increased, but the protein content of the livers decreased, in rats given histidine supplements. The histidine was associated with significantly higher folate concentrations in the livers of cyanocobalamin-supplemented rats.