The significance of the dilated renal pelvis in the nitrofen-exposed rat fetus: Effects on morphology and function

Kavlock, Robert J.; Hoyle, Blair R.; Rehnberg, Blair F.; Rogers, Ellen H.

doi:10.1016/0041-008x(88)90270-0

Cited by 8 publications

(6 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings rule out any possible direct stimulus from the lungs to the kidneys because, in that case, we should have found a marked difference in the measured parameters in the kidneys from the CDH group. A variable rate of ureterohydronephrosis has been reported in the nitrofen model of CDH [12][13][14]. We believe the inclusion of such cases could distort the actual kidney-to-body weight relationship as other authors have also suggested [6].…”

Section: Discussionmentioning

confidence: 81%

Kidney development in the nitrofen-induced pulmonary hypolasia and congenital diaphragmatic hernia in rats

Montedónico

Nakazawa

Shinkai

et al. 2007

Journal of Pediatric Surgery

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 81%

Kidney development in the nitrofen-induced pulmonary hypolasia and congenital diaphragmatic hernia in rats

Montedónico

Nakazawa

Shinkai

et al. 2007

Journal of Pediatric Surgery

View full text Add to dashboard Cite

“…Smaoui et al [34] studied the effects on the development of the glomerular basement membrane (GBM) of juxtamedullary nephrons in 1-day-old rat pups: myeloid bodies were found in podocytes, and the GBM appeared thicker and denser, and was abnormally permeable to ferritin and proteins. Chahoud et al [35] provided the first evidence of long-term functional and morphological changes in the rat kidney following prenatal treatment with gentamicin (110 mg /kg bw on GD 10-15 or [15][16][17][18][19][20]. One year later, the offspring showed reduced survival and increased systolic arterial pressure and urea plasma concentrations, particularly in females.…”

Section: Aminoglycosides and Other Antibioticsmentioning

confidence: 95%

“…Exposure during the fetal phase (GD [15][16][17][18][19][20] led to modest signs of overt neonatal toxicity; however, pups showed a decreased cardiac weight and histopathological changes of the kidneys, including medial hypertrophy of intracortical arterioles and dilatation of the renal pelvis. While the cardiac and renal vascular effects disappeared with time, renal lesions were still evident by PD 90.…”

Section: Angiotensin-converting Enzyme (Ace) Inhibitors and Related Dmentioning

confidence: 97%

“…Kavlock et al [20] already suggested that offspring should be monitored during postnatal development when alterations of the fetal renal papilla are observed in standard teratology bioassays, in order to determine whether the effect is transient or permanent. Understanding functional maturation is a keypoint for renal developmental toxicity.…”

Section: Drugs Affecting Renal Development the Development Of The Kidneymentioning

confidence: 98%

“…It is well known that hypothalamic catecholaminergic neurons play an important role in modulating the general omeostatic response of the organism to environmental stressors, that include enhanced NE turnover at the brain level and increased levels of corticosterone and prolactin in the general circulation. Thus, central and peripheral response to restraint stress were evaluated in adult rats exposed prenatally to DZ (dose range 1-10 mg/kg) over gestational days [13][14][15][16][17][18][19][20]. Prenatal exposure to DZ altered both the brain's intrinsic response to stress (i.e.…”

Section: Benzodiazepinesmentioning

confidence: 99%

See 2 more Smart Citations

Delayed Developmental Effects Following Prenatal Exposure to Drugs

Mantovani¹,

Calamandrei

2001

CPD

View full text Add to dashboard Cite

Increasing evidence points to the possible risks of delayed effects upon prenatal exposure to chemicals; the evaluation of such effects may pose serious problems to clinicians, epidemiologists and toxicologists. In fact, several systems (e.g., nervous, excretory) show important developmental processes well after the organogenetic period, up to the postnatal phase; accordingly, these are also expected to be sensitive targets of developmental toxicants, resulting in impairment of the function and/or functional reserve. This review describes the effects of several groups of drugs on the functional maturation and histogenesis of the kidney (e.g., aminoglycosides, angiotensin-converting enzyme inhibitors, indomethacin) and brain (e.g., anticonvulsivants, antiretroviral compounds, benzodiazepines) upon exposure in utero of humans and laboratory animals. The available data stress the importance for risk assessment of an adequate knowledge of both developmental biology and mechanisms of toxicity. The design of developmental toxicity studies should allow an evaluation of targets most relevant for a given drug (or group of drugs); moreover, the analysis of functional development should receive the due attention within the safety assessment of chemicals.

show abstract

Pre- and Postnatal Toxicity of the HMG-CoA Reductase Inhibitor Atorvastatin in Rats

Henck¹

1998

Toxicological Sciences

View full text Add to dashboard Cite

Atorvastatin is a potent inhibitor of the enzyme 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, which catalyzes the conversion of HMG-CoA to mevalonate and constitutes the rate-limiting step in the biosynthesis of cholesterol. Steroid hormones derived from cholesterol, as well as mevalonate and its isoprenoid derivatives, provide important contributions to the maternal animal during pregnancy and lactation, as well as to the growth and development of the offspring; these contributions may potentially be influenced by inhibition of HMG-CoA reductase. To investigate the effects of atorvastatin on various aspects of reproduction and development, female Sprague-Dawley rats received 0, 20, 100, or 225 mg/kg daily by gavage from gestation day 7 through lactation day 20. Maternal toxicity, characterized by morbidity/mortality (13%), reduced body weight gain and food consumption, and pathologic lesions in the nonglandular mucosa of the stomach, occurred at 225 mg/kg. Offspring survival at birth and during the neonatal period at 225 mg/kg was reduced relative to control by up to 45%, and 28% of litters had no viable offspring by 10 days postpartum. Additional effects on offspring included reduced body weight during the neonatal and maturation periods (100, 225 mg/kg), delayed appearance of pinnae detachment and incisor eruption (225 mg/kg), impaired rotorod performance (females only; 100, 225 mg/kg), reduced acoustic startle responding (males only; 20, 100, 225 mg/kg), and transient effects on shuttle avoidance (females only; 225 mg/kg). No treatment-related effects were observed on offspring reproduction. In a separate experiment, a single dose of 10 mg/kg atorvastatin administered to female Wistar rats on gestation day 19 or lactation day 13 provided evidence of placental transfer and excretion into the milk. Results of this study indicate that pre- and postnatal administration of atorvastatin to female rats produces developmental toxicity in their offspring via in utero and/or lactational exposure, and in the presence or absence of maternal toxicity.

show abstract

The significance of the dilated renal pelvis in the nitrofen-exposed rat fetus: Effects on morphology and function

Cited by 8 publications

References 6 publications

Kidney development in the nitrofen-induced pulmonary hypolasia and congenital diaphragmatic hernia in rats

Kidney development in the nitrofen-induced pulmonary hypolasia and congenital diaphragmatic hernia in rats

Delayed Developmental Effects Following Prenatal Exposure to Drugs

Pre- and Postnatal Toxicity of the HMG-CoA Reductase Inhibitor Atorvastatin in Rats

Contact Info

Product

Resources

About