Vitamin brain

DESRUMAUX, C., RISOLD, P. Y, SCHROEDER, H., DECKERT, V., MASSON, D., ATHIAS, A., LAPLANCHE, H., LE GUERN, N., BLACHE, D., JIANG, X. C., TALL, A. R., DESOR, D. LAGROST, L. 2005. Phospholipid transfer protein (PLTP) deficiency reduces brain vitamin E content and increases anxiety in mice. FASEB J, 19, 296-7. 

Calbindins are hormonally controlled by vitamin D and are expressed in the kidney, intestine, and brain. 

Ascorbic acid is photosensitive and unstable in aqueous solution at room temperature. During storage of foods, vitamin C is inactivated by oxygen. This process is accelerated by heat and the presence of catalysts. Ascorbic acid concentration in human organs is highest in adrenal and pituitary glands, eye lens, liver, spleen, and brain. Potatoes, citrus fruits, blade currants, sea buckthorns, acerola, rose hips, and red paprika peppers are among the most valuable vitamin C sources [1,2]. 

Particular attention is given to the development of new mechanistic biomarker assays and bioassays that can be used as indices of the toxicity of mixtures. These biomarker assays are typically based on toxic mechanisms such as brain acetylcholinesterase inhibition, vitamin K antagonism, thyroxin antagonism, Ah-receptor-mediated toxicity, and interaction with the estrogenic receptor. They can give integrative measures of the toxicity of mixtures of compounds where the components of the mixture share the same mode of action. They can also give evidence of potentiation as well as additive toxicity. 

The two major sites of P-carotene conversion are the intestine and liver in hnmans. The liver seems to have a greater capacity for metabolizing P-carotene to vitamin A than the intestine. " In rats, BCO activity was also reported to be higher in the small intestine and liver, followed by brain, Inng, and kidney. In agreement with the tissne distribntion of BCO activity, high levels of hnman BCO mRNA were reported in the jejnnnm, liver, and kidney, whereas lower levels were present in the prostate, testes, ovaries, and skeletal mnscles. 

Mammals lack the ability to synthesize astaxanthin or convert dietary astaxanthin into vitamin A. Unlike p-carotene, astaxanthin has no pro-vitamin activity in these animals. Astaxanthin has been shown in both in vitro and in a study with human subjects to be effective for the prevention of the oxidation of low-density protein, suggesting that it can be used to prevent arteriosclerosis, coronary artery disease, and ischemic brain development. A number of astaxanthin health products are under study. 

The free-radical defence mechanisms utilized by the brain are similar to those found in other tissues. The enzymes SOD, catalase, glutathione peroxidase, and the typical radical scavengers, ascorbate, vitamin E and vitamin A are present in the brain, as they are in peripheral tissues. However, the brain may actually be slightly deficient in some of these defence mechanisms when compared to the amounts present in other tissues. 

Sato, P.H. and Hall, E.D. (1992). Tirilazad mesylate protects vitamins C and E in brain ischemia-reperfasion injury. J. Neurochem. 58, 2263-2268. 

Hydroxydopamine (6-OHDA) is a neurotoxin that destroys catecholaminergic neurons in the brain. This toxicity is believed to be related to the production of ROS by the neurotoxin. Rats were fed chronically with vitamin E and then challenged with 6-OHDA. The usual depletion of SOD and reduced glutathione (GSH) in most brain regions was attenuated by the vitamin E pretreatment. The authors attributed this success to scavenging by the augmented brain levels of vitamin E (Perumal et al., 1992). 

Perumal, A.S., Gopal, V.B., Tordzro, W.K., Cooper, T.B. and Cadet, J.L. (1992). Vitamin E attenuates the toxic effects of 6-hydrooxydopamine on free radical scavenging systems in rat brain. Brain Res. Bull. 29, 699-701. 

Deficiency of manganese may lead to vitamin K deficiency (Chiswell and Johnson 1994) and to problems in prenatal and neonatal development of the brain. 

An example of the prognostic meaning of vitamin C measurements is given in Figure 13 [33], In this study on neurosurgical patients drastic reduction of the vitamin C concentration in blood during the operation was associated with postoperative brain edema. 

Classic antioxidants, vitamin E, vitamin C, and others can suppress the activation of apoptosis. For example, ascorbic acid prevented cytochrome c release and caspase activation in human leukemia cells exposed to hydrogen peroxide [128], Pretreatment with A -acctylcystcinc, ascorbate, and vitamin E decreased homocysteine thiolactone-induced apoptosis in human promyelocytic leukemia HL-60 cells [129]. Resveratrol protected rat brain mitochondria from anoxia-reoxygenation damage by the inhibition of cytochrome c release and the reduction of superoxide production [130]. However, it should be mentioned that the proapoptotic effect of ascorbate, gallic acid, or epigallocatechin gallate has been shown in the same human promyelocytic leukemia cells [131]. 

Levodopa is converted to dopamine in the peripheral tissues by dopa decarboxylase, which has pyridoxine as a cofactor. Excess of this vitamin will increase this reaction, which is an undesirable effect because dopamine does not cross the blood-brain barrier where the therapeutic effect is desired. 

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