Genetic effects of contaminant exposure - Towards an assessment of impacts on animal populations

被引:41
作者
Hebert, PDN [1 ]
Luiker, MM [1 ]
机构
[1] EVS CONSULTANTS LTD, N VANCOUVER, BC V7P 2R4, CANADA
基金
加拿大自然科学与工程研究理事会;
关键词
nuclear genome; mitochondrial genome; DNA; genetic diversity; mutagenesis; contaminant exposure;
D O I
10.1016/0048-9697(96)05169-8
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
This review aims both to identify the potential risks to animal populations as a consequence of exposure to genotoxins and to identify the techniques most useful in assessing these risks. These evaluations are complicated by the fact that contaminant exposure acts both to restructure naturally occurring genetic diversity and, when contaminants have mutagenic activity, to enhance the rate of introduction of new variation. There is now evidence that contaminant exposure often leads to change in the genetic attributes of natural populations. Short-lived organisms often develop resistance to contaminants, with only modest impacts on diversity in the balance of the genome, although massive mortality occurs during the gene replacement. Resistance is, however, less likely to evolve in species with small population sizes, such as many wildlife species. Such species will experience population declines or extinction as the impact of contaminants on physiological systems is not counteracted by gene replacements. Even when adaptation to exposure occurs, populations may suffer diminished fitness as a consequence of the mutagenic effects of contaminants. The expression of these effects range from an increase in the incidence of developmental abnormalities to shifts in chromosomal and gene structure. The assessment of this broad range of impacts can only be accomplished with a spectrum of analytical approaches. However, recent advances in molecular and developmental genetics are now making possible the detailed assessment of these mutagenic impacts in natural populations.
引用
收藏
页码:23 / 58
页数:36
相关论文
共 282 条
[1]  
AL-SABTI K, 1992, Cytobios, V70, P101
[2]   WHY USE SOMATIC MUTATIONS FOR HUMAN BIOMONITORING [J].
ALBERTINI, RJ .
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1994, 23 :18-22
[3]   ALTERATIONS OF THE HPRT GENE IN HUMAN INVIVO-DERIVED 6-THIOGUANINE-RESISTANT LYMPHOCYTES-T [J].
ALBERTINI, RJ ;
ONEILL, JP ;
NICKLAS, JA ;
HEINTZ, NH ;
KELLEHER, PC .
NATURE, 1985, 316 (6026) :369-371
[4]   DEVELOPMENT OF A RAPID AND SIMPLE GENOTOXICITY ASSAY USING A BROWN BULLHEAD FISH CELL-LINE - APPLICATION TO TOXICOLOGICAL SURVEYS OF SEDIMENTS IN THE HURON-ERIE CORRIDOR [J].
ALI, F ;
LAZAR, R ;
HAFFNER, D ;
ADELI, K .
JOURNAL OF GREAT LAKES RESEARCH, 1993, 19 (02) :342-351
[5]  
ALINK GM, 1982, MUTAGENS OUR ENV
[6]   COVALENT BINDING OF POLYCYCLIC AROMATIC-COMPOUNDS TO MITOCHONDRIAL AND NUCLEAR-DNA [J].
ALLEN, JA ;
COOMBS, MM .
NATURE, 1980, 287 (5779) :244-245
[7]   MICRONUCLEI INDUCED BY SELENIUM, MERCURY, METHYLMERCURY AND THEIR MIXTURES IN BINUCLEATED BLOCKED FISH ERYTHROCYTE CELLS [J].
ALSABTI, K .
MUTATION RESEARCH, 1994, 320 (1-2) :157-163
[8]   CARCINOGENS ARE MUTAGENS - SIMPLE TEST SYSTEM COMBINING LIVER HOMOGENATES FOR ACTIVATION AND BACTERIA FOR DETECTION [J].
AMES, BN ;
DURSTON, WE ;
YAMASAKI, E ;
LEE, FD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1973, 70 (08) :2281-2285
[9]   OXIDANTS, ANTIOXIDANTS, AND THE DEGENERATIVE DISEASES OF AGING [J].
AMES, BN ;
SHIGENAGA, MK ;
HAGEN, TM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (17) :7915-7922
[10]   CHROMOSOME ABERRATION AND SISTER CHROMATID EXCHANGE TEST-RESULTS WITH 42 CHEMICALS [J].
ANDERSON, BE ;
ZEIGER, E ;
SHELBY, MD ;
RESNICK, MA ;
GULATI, DK ;
IVETT, JL ;
LOVEDAY, KS .
ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, 1990, 16 :55-137