Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development

被引:36
作者
Crowe, A [1 ]
Morgan, EH [1 ]
机构
[1] UNIV WESTERN AUSTRALIA, DEPT PHYSIOL, PERTH, WA 6907, AUSTRALIA
关键词
transferrin; brain; kidney; growth;
D O I
10.1007/BF02789166
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Environmental lead intoxication, which frequently causes neurological disturbances, and iron deficiency are clinical problems commonly found in children. Also, iron deficiency has been shown to augment lead absorption from the intestine. Hence, there is evidence for an interaction between lead and iron metabolism which could produce changes in lead and iron uptake by the brain and other tissues. These possibilities were investigated using 15-, 21-, and 63-old rats with varying nutritional iron and lead status. Darns were fed diets containing 0 or 3% lead-acetate and 0.2% lead-acetate in the drinking water. After weaning, 0.2% lead-acetate in the drinking water became the sole source of dietary lead. Measurements were made of tissue lead and nonheme iron levels and the uptake of Fe-59 after intravenous injection of transferrin-bound Fe-59. Iron deficiency was associated with increased intestinal absorption of lead as indicated by blood and kidney lead levels in rats exposed to dietary lead. However, iron deficiency did not increase lead deposition in the brain, and in all rats brain lead levels were relatively low ( < 0.1 mu g/g). Lead concentrations in the liver were below 2 mu g/g, whereas kidneys had almost 20 times this concentration. Animals with iron deficiency had lower liver iron levels and had increased brain Fe-59 uptake in comparison to control rats. However, iron levels in brain and kidneys were unaffected by lead intoxication regardless of the animal's iron status. Fe-59 uptake rates were also unaffected by lead, but increased rates of uptake were apparent in iron-deficient rats. Lead did increase liver iron levels in all iron-adequate rats, but iron deficiency had little effect. It is concluded that, compared with other tissues, the blood-brain barrier largely restricts lead uptake by the brain and that the uptake tl-lat does occur is unrelated to the iron status of the animal. Also, the level of lead intoxication produced in this investigation did not influence iron uptake by the brain and kidneys, but liver iron stores could be increased if iron levels were already adequate.
引用
收藏
页码:249 / 261
页数:13
相关论文
共 27 条
[1]   LEAD POISONING AND HEMOGLOBIN SYNTHESIS - REPORT OF A STUDY OF 15 PATIENTS WITH CHRONIC LEAD INTOXICATION [J].
BOYETT, JD ;
BUTTERWORTH, CE .
AMERICAN JOURNAL OF MEDICINE, 1962, 32 (06) :884-&
[2]  
BRADBURY MWB, 1986, ANN NY ACAD SCI, V481, P142
[3]   TRANSPORT OF PB-203 AT THE BLOOD-BRAIN-BARRIER DURING SHORT CEREBROVASCULAR PERFUSION WITH SALINE IN THE RAT [J].
DEANE, R ;
BRADBURY, MWB .
JOURNAL OF NEUROCHEMISTRY, 1990, 54 (03) :905-914
[4]   VITAMIN E AND STRESS .3. METABOLISM OF D-ALPHA-TOCOPHEROL IN RAT UNDER DIETARY STRESS WITH SILVER [J].
DIPLOCK, AT ;
GREEN, J ;
BUNYAN, J ;
MCHALE, D ;
MUTHY, IR .
BRITISH JOURNAL OF NUTRITION, 1967, 21 (01) :115-&
[5]   EFFECT OF EXPOSURE TO LEAD ON MATURATION OF INTESTINAL IRON-ABSORPTION OF RATS [J].
DOBBINS, A ;
JOHNSON, DR ;
NATHAN, P .
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH, 1978, 4 (04) :541-550
[6]   COMPARATIVE EFFECTS OF IRON-DEFICIENCY INDUCED BY BLEEDING AND A LOW-IRON DIET ON THE INTESTINAL ABSORPTIVE INTERACTIONS OF IRON, COBALT, MANGANESE, ZINC, LEAD AND CADMIUM [J].
FLANAGAN, PR ;
HAIST, J ;
VALBERG, LS .
JOURNAL OF NUTRITION, 1980, 110 (09) :1754-1763
[7]   MECHANISMS OF KIDNEY-CELL INJURY FROM METALS [J].
FOWLER, BA .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1993, 100 :57-63
[8]   TRANSFERRIN AND IRON UPTAKE BY LIVER IN RAT [J].
GARDINER, ME ;
MORGAN, EH .
AUSTRALIAN JOURNAL OF EXPERIMENTAL BIOLOGY AND MEDICAL SCIENCE, 1974, 52 (OCT) :723-736
[9]   LEAD POISONING AND HEME BIOSYNTHESIS [J].
GOLDBERG, A .
BRITISH JOURNAL OF HAEMATOLOGY, 1972, 23 (05) :521-+
[10]  
HASHMI NS, 1989, BIOL TRACE ELEM RES, V22, P287, DOI 10.1007/BF02916617