			Home About us Contact

Embryonic Malformations (embryonic + malformation)

Distribution by Scientific Domains

Life Sciences	100%

Selected Abstracts

Cooler temperatures increase sensitivity to ultraviolet B radiation in embryos and larvae of the frog Limnodynastes peronii

GLOBAL CHANGE BIOLOGY, Issue 6 2007
VINCENT O. Van UITREGT
Abstract Recent studies suggest that complex interacting processes are driving global amphibian declines. Increased ultraviolet B (UVB) radiation in the solar spectrum associated with ozone depletion has been implicated in declines, and evidence suggests that the effects of UVB radiation on amphibians may be greater at cooler temperatures. We tested the thermal sensitivity of UVB effects on amphibians in a controlled factorial experiment using the striped marsh frog, Limnodynastes peronii as a model species. We compared survival, growth and locomotor performance of embryonic and larval L. peronii reared under low and high UVB exposures at both 20 and 30 °C. Embryonic and larval L. peronii proved extremely sensitive to UVB damage and exhibited greater sensitivity at 20 °C compared with 30 °C. Embryonic survival to Gosner stage 25 was unaffected by UVB exposure at 30 °C, but at 20 °C survival was reduced to 52% under high UVB. Larval survival exhibited a similar trend. At 20 °C, all tadpoles survived under low UVB, whereas under high UVB there was 100% mortality after 15 days of exposure. At 30 °C, 86% survived under low UVB, but only 46% survived under high UVB. Sublethal effects such as, embryonic malformation, retarded larval growth and reduced larval swimming performance were also greater at 20 °C compared with 30 °C. Our results strongly indicate that UVB damage in amphibians is markedly increased at cooler temperatures. Thus, populations of UVB sensitive species occurring at cold climates may be at greater risk of declines due to increased solar UVB radiation. [source]

Diabetic embryopathy: Studies using a rat embryo culture system and an animal model

CONGENITAL ANOMALIES, Issue 3 2005
Shoichi Akazawa
ABSTRACT The mechanism of diabetic embryopathy was investigated using in vitro experiments in a rat embryo culture system and in streptozotocin-induced diabetic pregnant rats. The energy metabolism in embryos during early organogenesis was characterized by a high rate of glucose utilization and lactic acid production (anaerobic glycolysis). Embryos uninterruptedly underwent glycolysis. When embryos were cultured with hypoglycemic serum, such embryos showed malformations in association with a significant reduction in glycolysis. In a diabetic environment, hyperglycemia caused an increased glucose flux into embryonic cells without a down-regulation of GLUT1 and an increased metabolic overload on mitochondria, leading to an increased formation of reactive oxygen species (ROS). Activation of the hexamine pathway, subsequently occurring with increased protein carbonylation and increased lipid peroxidation, also contributed to the increased generation of ROS. Hyperglycemia also caused a myo-inositol deficiency with a competitive inhibition of ambient glucose, which might have been associated with a diminished phosphoinositide signal transduction. In the presence of low activity of the mitochondrial oxidative glucose metabolism, the ROS scavenging system in the embryo was not sufficiently developed. Diabetes further weakened the antioxidant system, especially, the enzyme for GSH synthesis, ,-GCS, thereby reducing the GSH concentration. GSH depletion also disturbed prostaglandin biosynthesis. An increased formation of ROS in a diminished GSH-dependent antioxidant system may, therefore, play an important role in the development of embryonic malformations in diabetes. [source]

Cellular and molecular basis of cadmium-induced deformities in zebrafish embryos

ENVIRONMENTAL TOXICOLOGY & CHEMISTRY, Issue 12 2000
Shuk Han Cheng
Abstract Cadmium is known to cause developmental defects in a varietyof vertebrate species, but relatively little is known about the underlying molecular mechanisms. In this study, we used zebrafish (Danio rerio) embryos as a model system to investigate cadmium-induced toxicities. Fertilized embryos collected at 5-h after fertilization were incubated for 18 h in culture media containing 1 to 1, 000 ,M CdCl2. The median embryolethal concentration (LC50) was 168 ,M, whereas the median effect concentration (EC50) for total adverse effect (mortality and developmental defects) was 138 ,M. Six major types of deformities were observed: head and eye hypoplasia, hypopigmentation, cardiac edema, yolk sac abnormalities, altered axial curvature, and tail malformations. The frequency of malformations increased with cadmium concentration. Somites of embryos with altered axial curvature were investigated using the antimyosin antibody MF-20. This study demonstrated, to our knowledge for the first time, reduced myotome formation in cadmium-induced spinal deformity. Embryos with head and eye hypoplasia were studied using the anti-neural tissue antibody zns-2, and a poorly developed central nervous system was revealed. Head and eye hypoplasia were associated with lack of expression of the sonic hedgehog gene, which controls the patterning of the neural tube and somites. Genes involved in tail formations, such as evenskipped 1 and no tail, were ectopically expressed in embryos with tail malformations. Our data support the hypothesis that fish embryonic malformations induced by cadmium might be mediated through ectopic expression of developmental regulatory genes. [source]

Fetal cardiac effects of maternal hyperglycemia during pregnancy

BIRTH DEFECTS RESEARCH, Issue 6 2009
Niamh Corrigan
Maternal diabetes mellitus is associated with increased teratogenesis, which can occur in pregestational type 1 and type 2 diabetes. Cardiac defects and with neural tube defects are the most common malformations observed in fetuses of pregestational diabetic mothers. The exact mechanism by which diabetes exerts its teratogenic effects and induces embryonic malformations is unclear. Whereas the sequelae of maternal pregestational diabetes, such as modulating insulin levels, altered fat levels, and increased reactive oxygen species, may play a role in fetal damage during diabetic pregnancy, hyperglycemia is thought to be the primary teratogen, causing particularly adverse effects on cardiovascular development. Fetal cardiac defects are associated with raised maternal glycosylated hemoglobin levels and are up to five times more likely in infants of mothers with pregestational diabetes compared with those without diabetes. The resulting anomalies are varied and include transposition of the great arteries, mitral and pulmonary atresia, double outlet of the right ventricle, tetralogy of Fallot, and fetal cardiomyopathy. A wide variety of rodent models have been used to study diabetic teratogenesis. Both genetic and chemically induced models of type 1 and 2 diabetes have been used to examine the effects of hyperglycemia on fetal development. Factors such as genetic background as well as confounding variables such as obesity appear to influence the severity of fetal abnormalities in mice. In this review, we will summarize recent data on fetal cardiac effects from human pregestational diabetic mothers, as well as the most relevant findings in rodent models of diabetic cardiac teratogenesis. Birth Defects Research (Part A), 2009. © 2009 Wiley-Liss, Inc. [source]