PATHOPHYSIOLOGICAL ASPECTS OF INTOXICATION WITH CYANOGEN SUBSTANCES

被引:0
作者
Lilios, Gabriela [1 ]
Taralunga, Gheorghe [1 ]
Arcus, Mariana [1 ]
Stoicescu, Ramona M. [1 ]
Schroder, Verginica [1 ]
机构
[1] Ovidius Univ Constanta, Fac Pharm, Constanta, Romania
来源
PSYCHOLOGY AND PSYCHIATRY, SOCIOLOGY AND HEALTHCARE, EDUCATION, VOL II | 2014年
关键词
cyanogen substances; thyroid gland; thiocyanides; intoxication; CYANIDE;
D O I
暂无
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
The highest quantity of cyanogen compounds in the environment results mainly from human activities (ore extraction, cleaning and hardening metals, galvanization etc). People with metabolic disorders in cyanide conversion to thiocyanide show a higher risk of intoxication with cyanogen substances. Some deficient diets may increase the risk to cyanide exposure. Thiocyanide, the main metabolite of cyanide, cause endemic goiter in humans and animals. In the studies, orally administrated cyanide and thiocyanide to rats, induced effects on the thyroid gland. The mechanisms through which the cyanides induce effects on the thyroid gland are demonstrated that thiocyanide significantly inhibited the accumulation of iodine in the thyroid gland, lowering the ability of this gland to keep the iodine concentration above the blood concentration. Moreover, thiocyanide may inhibit the iodine fixing, thus interfering the organic iodine binding at glandular level. In the cyanogen intoxication, the para clinical examinations can be classified into two groups: laboratory examinations that aim to determine certain biochemical and hematologic modifications and laboratory examinations that determine the toxicants in the organism or reveal their metabolism products. The analytical toxicological diagnosis is both qualitative, identifying the cyanogen toxicant involved in the intoxication etiology, and quantitative, establishing the cyanide concentration in the biological fluids, in order to estimate the quantity of the toxic substance in the organism and to assess the severity and the evolution of the intoxication. In spite of numerous sources which can release cyanides into the environment, the available data are few, that is why the average daily value of cyanides that enter the human organism has not been able to be evaluated.
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页码:623 / 628
页数:6
相关论文
共 11 条
[1]   CYANIDE INTOXICATION AMONG SILVER-RECLAIMING WORKERS [J].
BLANC, P ;
HOGAN, M ;
MALLIN, K ;
HRYHORCZUK, D ;
HESSL, S ;
BERNARD, B .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1985, 253 (03) :367-371
[2]  
Doherty P. J., 1982, J BIOL CHEM, V257
[3]   Mice Deficient in Dual Oxidase Maturation Factors Are Severely Hypothyroid [J].
Grasberger, Helmut ;
De Deken, Xavier ;
Mayo, Olga Barca ;
Raad, Houssam ;
Weiss, Mia ;
Liao, Xiao-Hui ;
Refetoff, Samuel .
MOLECULAR ENDOCRINOLOGY, 2012, 26 (03) :481-492
[4]   A Single Copy of the Recently Identified Dual Oxidase Maturation Factor (DUOXA) 1 Gene Produces Only Mild Transient Hypothyroidism in a Patient with a Novel Biallelic DUOXA2 Mutation and Monoallelic DUOXA1 Deletion [J].
Hulur, Imge ;
Hermanns, Pia ;
Nestoris, Claudia ;
Heger, Sabine ;
Refetoff, Samuel ;
Pohlenz, Joachim ;
Grasberger, Helmut .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2011, 96 (05) :E841-E845
[5]  
Kreutler P. A., 1977, AM J CLIN NUTR, V31, P282
[6]   Cell biology of H2O2 generation in the thyroid: Investigation of the control of dual oxidases (DUOX) activity in intact ex vivo thyroid tissue and cell lines [J].
Massart, C. ;
Hoste, C. ;
Virion, A. ;
Ruf, J. ;
Dumont, J. E. ;
Van Sande, J. .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 2011, 343 (1-2) :32-44
[7]  
Niculescu T., 1985, MANUAL PATOLOGIE PRO, VI, P509
[8]   EFFECTS OF PROLONGED CYANIDE AND THIOCYANATE FEEDING IN RATS [J].
PHILBRICK, DJ ;
HOPKINS, JB ;
HILL, DC ;
ALEXANDER, JC ;
THOMSON, RG .
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH, 1979, 5 (04) :579-592
[9]   EFFECTS OF THIOSULFATE ON CYANIDE PHARMACOKINETICS IN DOGS [J].
SYLVESTER, DM ;
HAYTON, WL ;
MORGAN, RL ;
WAY, JL .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1983, 69 (02) :265-271
[10]  
WILSON J, 1987, CLIN EXPT TOXICOLOGY, P292