Sivakumar B
Division of Biophysics, National Institute of Nutrition (ICMR), Hyderabad.
Indian J Med Res. 1998 Nov;108:157-66.
Most of the dietary vitamin A is derived from plant foods in the form of pro-vitamin A, the carotenoids. Though in 1930 it was first demonstrated that beta-carotene is the precursor for vitamin A and it is well accepted that 1 mole of beta-carotene is equivalent to one mole of vitamin A, the mechanism of conversion to vitamin A has been controversial. Some of the mechanisms suggested are central cleavage potentially yielding 2 molecules of vitamin A or excentric cleavage producing one molecule of vitamin A from beta-carotene which drastically varied the potency of carotene. A mucosal supernatant from rat intestine was shown to have beta-carotene dioxygenase activity which provided the basis for central cleavage. Many observations on enzyme activity in vitro and efficacy of carotene in vivo did not support the above findings and a re-evaluation of the whole problem was undertaken at the National Institute of Nutrition (NIN), Hyderabad. Intestinal conversion of beta-carotene to vitamin A both in vitro and in vivo in rats and in vivo in children was evaluated. A novel method of obtaining the in vivo conversion of carotene to vitamin A using the ratio of area under plasma vitamin A time curves after a dose of beta-carotene and vitamin A (> 100 micrograms) was developed in rats and later extended to children. In children a dose of 1.5 mg of beta-carotene and vitamin A was used. From these studies intestinal conversion of beta-carotene to vitamin A was found to be an enzymatic reaction involving central cleavage and which needed the presence of oxygen. The substrate was found to bind the enzyme at C-15,15'. The enzyme may be associated with inherent or contaminant enzyme which breaks of other part of the molecule released after central cleavage of carotene. The in vivo conversion of carotene to vitamin A was found to vary from 20 to 80 per cent depending on the nutritional status. Vitamin A deficiency was found to enhance both the in vitro and in vivo conversion and protein deficiency to decrease both. Thus the present results confirm the convertibility of dietary carotenoids to vitamin A and could facilitate further investigations on interactions of different dietary carotenoids on the absorption and cleavage of carotene to vitamin A in children.
大多数膳食维生素A以维生素A原(类胡萝卜素)的形式来源于植物性食物。尽管1930年首次证明β-胡萝卜素是维生素A的前体,且人们普遍认为1摩尔β-胡萝卜素等同于1摩尔维生素A,但向维生素A转化的机制一直存在争议。提出的一些机制包括可能产生2分子维生素A的中心裂解,或从β-胡萝卜素产生1分子维生素A的偏心裂解,这极大地改变了胡萝卜素的效力。大鼠肠道的黏膜上清液显示具有β-胡萝卜素双加氧酶活性,这为中心裂解提供了依据。许多关于体外酶活性和胡萝卜素体内功效的观察结果并不支持上述发现,海得拉巴德国家营养研究所(NIN)对整个问题进行了重新评估。评估了大鼠体内外以及儿童体内β-胡萝卜素向维生素A的肠道转化情况。在大鼠中开发了一种利用给予β-胡萝卜素和维生素A(>100微克)后血浆维生素A时间曲线下面积之比来获得胡萝卜素向维生素A体内转化的新方法,该方法后来扩展到了儿童。在儿童中使用了1.5毫克的β-胡萝卜素和维生素A剂量。从这些研究中发现,β-胡萝卜素向维生素A的肠道转化是一个涉及中心裂解的酶促反应,并且需要氧气的存在。发现底物在C-15,15'处与酶结合。该酶可能与内在或污染性酶相关,后者会分解胡萝卜素中心裂解后释放的分子的其他部分。发现胡萝卜素向维生素A的体内转化因营养状况而异,范围在20%至80%之间。发现维生素A缺乏会增强体内外转化,而蛋白质缺乏则会降低两者。因此,目前的结果证实了膳食类胡萝卜素可转化为维生素A,并有助于进一步研究不同膳食类胡萝卜素对儿童胡萝卜素吸收和裂解为维生素A的相互作用。