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Micronuclei and developmental abnormalities in 4‐day mouse embryos after paternal treatment with acrylamide
Author(s) -
TitenkoHolland Nina,
Ahlborn Thomas,
Lowe Xiu,
Shang g,
Smith Martyn T.,
Wyrobek Andrew J.
Publication year - 1998
Publication title -
environmental and molecular mutagenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1
H-Index - 87
eISSN - 1098-2280
pISSN - 0893-6692
DOI - 10.1002/(sici)1098-2280(1998)31:3<206::aid-em2>3.0.co;2-i
Subject(s) - micronucleus test , embryo , acrylamide , biology , genetics , andrology , mutagen , toxicology , carcinogen , medicine , toxicity , chemistry , organic chemistry , copolymer , polymer
The developmental consequences of paternal exposure to acrylamide (50 mg/kg i.p. for 5 days) were assessed in preimplantation embryos. There was a significant increase in the proportion of morphologically abnormal embryos after postmeiotic treatment during spermatogenesis (88.7% vs. 14.8% in control). Abnormal embryos had an average of 1.8 ± 3.5 cells and >80% had at least one fragmented nucleus. In addition, morphologically normal embryos were significantly delayed (34.3 ± 12.8 cells per embryo vs. 57.6 ± 15.7 in control, P < 0.001). Acrylamide caused 10‐ and 20‐fold increases in frequencies of cells with micronuclei (MN) in morphologically normal and abnormal embryos, respectively (41 and 93 MN per 1,000 cells). Both centromere‐negative (M−) and centromere‐positive (M+) were induced. Nuclei of abnormal embryos were significantly larger (900 μm 2 vs. 250 μm 2 ) than controls. In addition, MN of abnormal embryos were larger than those of normal embryos (21.2 μm 2 vs. 6.5 μm 2 , P < 0.01). Among control embryos, M+ were significantly larger than M− ( P < 0.05). These findings suggest that the preimplantation embryo is a sensitive indicator of paternally transmitted effects on early development. Multiple mechanisms appear to be involved, including cytogenetic damage, proliferation arrest/delay, and fertilization failure. Future studies are needed to establish how induced cytological defects in preimplantation embryos contribute to birth defects and other postimplantation abnormalities. Environ. Mol. Mutagen. 31:206–217, 1998 © 1998 Wiley‐Liss, Inc.