Postao/la marijanama » 21 sij 2009, 14:25
Vitamin neurotoxicity.
Snodgrass SR.
Department of Neurology, University of Southern California, School of Medicine, Los Angeles 90033.
Vitamins contain reactive functional groups necessary to their established roles as coenzymes and reducing agents. Their reactive potential may produce injury if vitamin concentration, distribution, or metabolism is altered. However, identification of vitamin toxicity has been difficult. The only well-established human vitamin neurotoxic effects are those due to hypervitaminosis A (pseudotumor cerebri) and pyridoxine (sensory neuropathy). In each case, the neurological effects of vitamin deficiency and vitamin excess are similar. Closely related to the neurological symptoms of hypervitaminosis A are symptoms including headache, pseudotumor cerebri, and embryotoxic effects reported in patients given vitamin A analogs or retinoids. Most tissues contain retinoic acid (RA) and vitamin D receptors, members of a steroid receptor superfamily known to regulate development and gene expression. Vitamin D3 effects on central nervous system (CNS) gene expression are predictable, in addition to the indirect effects owing to its influence on calcium and phosphorus homeostasis. Folates and thiamine cause seizures and excitation when administered in high dosage directly into the brain or cerebrospinal fluid (CSF) of experimental animals but have rarely been reported to cause human neurotoxicity, although fatal reactions to i.v. thiamine are well known. Ascorbic acid influences CNS function after peripheral administration and influences brain cell differentiation and 2-deoxyglucose accumulation by cultured glial cells. Biotin influences gene expression in animals that are not vitamin-deficient and alters astrocyte glucose utilization. The multiple enzymes and binding proteins involved in regeneration of retinal vitamin A illustrate the complexity of vitamin processing in the body. Vitamin A toxicity is also a good general model of vitamin neurotoxicity, because it shows the importance of the ratio of vitamin and vitamin-binding proteins in producing vitamin toxicity and of CNS permeability barriers. Because vitamin A and analogs enter the CNS better than most vitamins, and because retinoids have many effects on enzyme activity and gene expression, Vitamin A neurotoxicity is more likely than that of most, perhaps all other vitamins. Megadose vitamin therapy may cause injury that is confused with disease symptoms. High vitamin intake is more hazardous to peripheral organs than to the nervous system, because CNS vitamin entry is restricted. Vitamin administration into the brain or CSF, recommended in certain disease states, is hazardous and best avoided. The lack of controlled trials prevents us from defining the lowest human neurotoxic dose of any vitamin. Large differences in individual susceptibility to vitamin neurotoxicity probably exist, and ordinary vitamin doses may harm occasional patients with genetic disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
NEUROLOGY 2008;71:447-451
© 2008 American Academy of Neurology
High levels / Overdose / Toxicity / Negative Side Effects - Symptoms and/or Risk Factors:
Folic Acid:Vitamin B12:
Kidney damage, abdominal bloating / distention,Can cause folic acid-related anemia if low,
nausea, loss of appetite, increased cholesterolnumbness or tingling in right arm or right side
LDL / HDL ratio, increased zinc and potassiumof face, anxieties, panic-anxiety attacks, heart
requirements, may mask pernicious anemiapalpitations, hyperthyroid, optic nerve atrophy
from Vitamin B12 deficiency, worsens some(in someone with Leber's disease), insomnia,
types of childhood leukemia,some types of leukemia, liver, kidney diseases,
may worsen symptoms of mitral valve prolapse,
may increase tumor / cancer cell division,
usput molim te napiši naslov onog tvog topića.
