Gestational and lactational lead intoxication produces alterations in the hepatic system of rat pups

被引:17
作者
Corpas, I [1 ]
Benito, MJ [1 ]
Marquina, D [1 ]
Castillo, M [1 ]
Lopez, N [1 ]
Antonio, T [1 ]
机构
[1] Univ Complutense, Dept Anim Biol 2, Madrid 28040, Spain
关键词
lead; liver; development; rats;
D O I
10.1006/eesa.2001.2102
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The effects of lead (Pb) intoxication during pregnancy and lactation were studied in the hepatic system of pups and young Wistar rats to test the hypothesis that gestational and lactational lead exposure alters the normal function of the liver in neonates. Lead acetate (300 mg/L) dissolved in distilled water was administered ad libitum to mothers during gestation and lactation. At days 12 and 21 postnatal (PN), pups were sacrificed, blood was collected, and livers were removed. Blood lead (PbB) levels were also measured. Although, histological evaluation revealed neither abnormalities in the liver structure nor depositions of lead, the toxicant produced biochemical alterations. Lead-intoxicated pups exhibited a decrease in hemoglobin, iron, and alkaline and acid phosphatase levels and an increase in PbB content. Protein, DNA, and lipid total amounts were reduced, and hepatic glycogen content was diminished at days 12 and 21 PN, with a higher level of glucose in the blood. Lead administration also resulted in a decrease in alkaline phosphatase in the liver of pups at day 21 PN, but acid phosphatase was unaltered. The findings of this study support the hypothesis that lead intoxication of mothers in gestation and lactation results in alterations in the hepatic system in neonates and pups. (C) 2002 Elsevier Science.
引用
收藏
页码:35 / 43
页数:9
相关论文
共 46 条
[1]   THE EFFECT OF ZINC-DEFICIENCY ON ALKALINE-PHOSPHATASE (EC-3.1.3.1) AND ITS ISOENZYMES [J].
ADENIYI, FA ;
HEATON, FW .
BRITISH JOURNAL OF NUTRITION, 1980, 43 (03) :561-569
[2]  
Antonio Garcia M. T., 1988, Environmental Technology Letters, V9, P227
[4]  
BONITHONKOPP C, 1986, BIOL RES PREG PERIN, V7, P37
[5]   ZINC AND COPPER IN TISSUES OF RATS WITH BLOOD HYPERTENSION INDUCED BY LONG-TERM LEAD-EXPOSURE [J].
BOSCOLO, P ;
CARMIGNANI, M ;
CARELLI, G ;
FINELLI, VN ;
GIULIANO, G .
TOXICOLOGY LETTERS, 1992, 63 (02) :135-139
[6]   LEAD-INDUCED CELL-PROLIFERATION AND ORGAN-SPECIFIC TUMORIGENICITY [J].
CALABRESE, EJ ;
BALDWIN, LA .
DRUG METABOLISM REVIEWS, 1992, 24 (03) :409-416
[7]   LEAD IN CEREBROSPINAL-FLUID AND ITS RELATIONSHIP TO PLASMA LEAD IN HUMANS [J].
CAVALLERI, A ;
MINOIA, C ;
CERONI, M ;
POLONI, M .
JOURNAL OF APPLIED TOXICOLOGY, 1984, 4 (02) :63-65
[8]   INVITRO ASSESSMENT OF THE TOXICITY OF METAL-COMPOUNDS .4. DISPOSITION OF METALS IN CELLS - INTERACTIONS WITH MEMBRANES, GLUTATHIONE, METALLOTHIONEIN, AND DNA [J].
CHRISTIE, NT ;
COSTA, M .
BIOLOGICAL TRACE ELEMENT RESEARCH, 1984, 6 (02) :139-158
[9]  
COLUMBANO A, 1987, CANCER RES, V47, P5557
[10]   APPARENT QUIESCENCE OF THE METALLOTHIONEIN GENE IN THE RAT VENTRAL PROSTATE - ASSOCIATION WITH CADMIUM-INDUCED PROSTATE TUMORS IN RATS [J].
COOGAN, TP ;
SHIRAISHI, N ;
WAALKES, MP .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1994, 102 :137-139