Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003969 (vitamin C deficiency)
 625 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Workers of two chemical plants exposed to chlorobenzene were examined for actual nutrition and effects of the treatment and prophylactic diet on the food status. Investigation of the actual nutrition has demonstrated that the energy value of the daily diets approaches the magnitudes established for the given occupational and age group whereas the daily distribution of food with respect to the caloric value and alimentary substances does not correspond to the hygienic standards. The treatment and prophylactic diets developed for the workers were also characterized by disproportion between the dietary components. As compared to the control group, the workers exposed to chlorobenzene demonstrated a lower content of total glutathione in blood plasma. The majority of the workers manifested ascorbic acid deficiency. In accordance with the study of the coefficients of the activation of erythrocytic enzymes, it may be concluded that the workers placed on the treatment and prophylactic diet are better provided with vitamins B1, B2 and B6 than the workers of the housing and communal services. Thirty percent of the workers showed vitamin B6 deficiency. This may have an adverse action on the resistance to industrial substances conjugating with glutathione. The rate of vitamin B1 deficiency was also fairly high, whereas in the workers of one of the plants the magnitude of the TDP-effect appeared higher than normal.
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PMID:[Actual nutrition and biochemical parameters of the food status of workers exposed to chlorobenzene]. 280 Apr 53

Effects of deficiency of vitamins on early development of brain have been reviewed. Unusual developmental problems in neurogenesis specific for the brain and impairment of its functional capacities due to vitamin deficiency have been discussed. The species-specific "critical periods" in development of various systems have been mentioned. Indices such as reflex activity, locomotion, special senses, cognition and adaptive behavior were used for assessing brain maturation in experimental models and humans. Significant examples include brain anomalies in humans and other mammals caused by retinoid excess or deficit; increase in calbindin D28K, a vitamin D dependent calcium-binding protein during postnatal period in rat; hydrocephalus and exencephaly in prenatal rats and subarachnoidal or intracerebral hemorrhage in infants caused by vitamin E deficiency. Peripheral neuropathic lesions leading to infantile beriberi is caused by thiamine deficiency. Impaired growth in retinal layers leading to delay in maturation of electroretinogram and depth-perception in postnatal rats occur due to pyridoxine deficiency. Infants of severely vitamin B12 deficient mothers show abnormalities in behavior involving basal ganglia and pyramidal tract. Folic acid deficiency results in delayed maturation of the basic electroencepalographic patterns. In addition, vitamin-interactions leading to developmental errors have been pointed out. Vitamin B6 deficiency impairs vitamin B12 absorption and biotin deficiency may be aggravated by pantothenic acid deficiency. Vitamin C deficiency resulting in impaired metabolism may produce symptoms of deficiency of folic acid. Another characteristic examples is that iron absorption from dietary sources is dependent on ascorbic acid.
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PMID:Vitamins and brain development. 1052 53