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Inappropriate use of albino animals as models in research

Identifieur interne : 003818 ( Main/Exploration ); précédent : 003817; suivant : 003819

Inappropriate use of albino animals as models in research

Auteurs : Donnell Creel [États-Unis]

Source :

RBID : ISTEX:1FB351139497BE50380801FA860C721BD9642BEB

English descriptors

Abstract

Abstract: Sensory-neural, biochemical-metabolic, and physiological anomalies occur in albino mammals. There are ontogenic and biochemical parallels between the senses, peripheral nervous system, endocrine glands, metabolism, and melanin pigmentation. All albino mammals examined have abnormal optic systems. Many drugs cannot be adequately evaluated in an albino model because of melanin's ability to bind and interact with some chemicals. There is evidence that a general reduction in melanin pigment is correlated with a paucity of amino acids necessary for normal chemical function of the brain. There is a high probability that enzyme levels indicative of metabolic performance are deficient in the liver and kidneys of albinos. Congenital defects are associated with hypopigmentation in animal models and human syndromes. Melanin is found in abundance in the eye, inner ear, and midbrain where neural impulses are initiated indicating a possible role as an electrophysiologic mechanism. Microwave irradiation differentially affects albino and pigmented animals. Implications of these observations and other reports of anomalies associated with hypopigmentation suggest caution in the use of albino and other hypomelanotic animals as normal models in biological research.

Url:
DOI: 10.1016/0091-3057(80)90461-X


Affiliations:


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Le document en format XML

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<term>Abnormality</term>
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<term>Albino gene</term>
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<term>Audiogenic seizures</term>
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<term>Behav</term>
<term>Biochem</term>
<term>Biol</term>
<term>Catecholamine</term>
<term>Chloroquine</term>
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<term>Congenital</term>
<term>Congenital deafness</term>
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<term>Devl biol</term>
<term>Dose levels</term>
<term>Expl</term>
<term>Genet</term>
<term>Guillery</term>
<term>Hepatic encephalopathy</term>
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<term>Iris</term>
<term>Mammal</term>
<term>Melanin</term>
<term>Melanin pigment</term>
<term>Melanin pigmentation</term>
<term>Metabolic</term>
<term>Metabolic pathways</term>
<term>Neurol</term>
<term>Nonagouti</term>
<term>Ophthal</term>
<term>Optokinetic nystagmus</term>
<term>Partial albinism</term>
<term>Pathway</term>
<term>Pentobarbital</term>
<term>Physiol</term>
<term>Pigmentation</term>
<term>Precursor</term>
<term>Psychol</term>
<term>Rat</term>
<term>Retinal pigment epithelium</term>
<term>Retinogeniculate projections</term>
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<term>Syndrome</term>
<term>Uncrossed</term>
<term>Visual pathways</term>
<term>Visual system anomalies</term>
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<div type="abstract" xml:lang="en">Abstract: Sensory-neural, biochemical-metabolic, and physiological anomalies occur in albino mammals. There are ontogenic and biochemical parallels between the senses, peripheral nervous system, endocrine glands, metabolism, and melanin pigmentation. All albino mammals examined have abnormal optic systems. Many drugs cannot be adequately evaluated in an albino model because of melanin's ability to bind and interact with some chemicals. There is evidence that a general reduction in melanin pigment is correlated with a paucity of amino acids necessary for normal chemical function of the brain. There is a high probability that enzyme levels indicative of metabolic performance are deficient in the liver and kidneys of albinos. Congenital defects are associated with hypopigmentation in animal models and human syndromes. Melanin is found in abundance in the eye, inner ear, and midbrain where neural impulses are initiated indicating a possible role as an electrophysiologic mechanism. Microwave irradiation differentially affects albino and pigmented animals. Implications of these observations and other reports of anomalies associated with hypopigmentation suggest caution in the use of albino and other hypomelanotic animals as normal models in biological research.</div>
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