Morphological changes in lungs, placenta, liver and kidneys of pregnant rats exposed to cigarette smoke

Czekaj, Piotr; Pałasz, Artur; Lebda-Wyborny, Tomasz; Nowaczyk-Dura, G; Karczewska, W.; Florek, Ewa; Kamiński, Marian

doi:10.1007/s00420-002-0343-3

Cited by 41 publications

(9 citation statements)

References 26 publications

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“…In the kidney, developmental CSE alters the shape of the proximal and distal convoluted tubules, reduces the proximal tubule cuboidal epithelium thickness, and yields immature glomeruli in neonates [64, 65]. As previously demonstrated, 'active' CSE during pre- and post-natal development, including the entirety of kidney organogenesis, results in low birth weight that is coupled to decreased offspring weights throughout postnatal development, although the rate of growth is unaffected [44].…”

Section: Discussionmentioning

confidence: 99%

Developmental cigarette smoke exposure II: Kidney proteome profile alterations in 6 month old adult offspring

Neal

Jagadapillai

Chen

et al. 2016

Reproductive Toxicology

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Cigarette smoke exposure (CSE) during gestation and early development suppresses the growth trajectory in offspring. In prior studies utilizing a mouse model of ‘active’ developmental CSE (GD1-PD21), low birth weight induced by CSE persisted throughout the neonatal period and was present at the cessation of exposure at weaning with proportionally smaller kidney mass that was accompanied by impairment of carbohydrate metabolism. In the present study, littermates of those characterized in the prior study were maintained until 6 months of age at which time the impact of developmental CSE on the abundance of proteins associated with cellular metabolism in the kidney was examined. Kidney protein abundances were examined by 2D-SDS-PAGE based proteome profiling with statistical analysis by Partial Least Squares-Discriminant Analysis. Key findings of this study include a persistence of impact of developmental CSE past the original exposure period on the nucleic acid and carbohydrate metabolism networks and oxidant scavenging pathways.

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Section: Discussionmentioning

confidence: 99%

Developmental cigarette smoke exposure II: Kidney proteome profile alterations in 6 month old adult offspring

Neal

Jagadapillai

Chen

et al. 2016

Reproductive Toxicology

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“…Both are positively associated with the development of hypertension (Abitbol and Ingelfinger, 2009). The putative link between developmental CSE and adult onset hypertension and/or cardiovascular disease may be attributed in part to mild structural dysmorphology and proportionally smaller kidney size (Czekaj et al ., 2002; Nelson et al ., 1999). In utero passive CSE at defined developmental windows (pre-, during, and post-organogenesis) induced growth retardation paired with increased kidney cellular apoptosis, delayed glomerular maturation, and mesenchymal histological abnormalities (Nelson et al ., 1999).…”

Section: Introductionmentioning

confidence: 99%

Developmental cigarette smoke exposure: Kidney proteome profile alterations in low birth weight pups

Jagadapillai

Chen²,

Canales³

et al. 2012

Toxicology

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The Brenner hypothesis states that a congenital reduction in nephron number predisposes to adult-onset hypertension and renal failure. The reduction in nephron number induced by proportionally smaller kidney mass may predispose offspring to glomerular hyperfiltration with maturity onset obesity. Developmental cigarette smoke exposure (CSE) results in intrauterine growth retardation with a predisposition to obesity and cardiovascular disease at maturity. Utilizing a mouse model of ‘active’ developmental CSE (gestational day [GD] 1-postnatal day [PD] 21; cotinine>50 ng/mL) characterized by persistently smaller offspring with proportionally decreased kidney mass, the present study examined the impact of developmental CSE on the abundance of proteins associated with cellular metabolism in the kidney. Following cessation of CSE on PD21, kidney tissue was collected from CSE and Sham exposed pups for 2D-SDS-PAGE based proteome profiling with statistical analysis by Partial Least Squares-Discriminant Analysis (PLS-DA) with affected molecular pathways identified by Ingenuity Pathway Analysis. Proteins whose expression in the kidney were affected by developmental CSE belonged to the inflammatory disease, cell to cell signaling/interaction, lipid metabolism, small molecule biochemistry, cell cycle, respiratory disease, nucleic acid and carbohydrate metabolism networks. The present findings indicate that developmental CSE alters the kidney proteome. The companion paper details the liver proteome alterations in the same offspring.

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“…The literature shows that metabolic acidosis may negatively impact bone metabolism 2 . In this study, the animals were exposed to passive smoking, which produces respiratory acidosis; 6 this may suggest that the changes seen in BMD and BMC may be connected to the effects of smoke exposure.…”

Section: Discussionmentioning

confidence: 82%

“…- Adaptation stage: the first five days of exposure to cigarette smoke for group G1 in the smoke chamber at a temperature of 23±1°C 6 for 10 minutes, once a day, with 250 ppm (parts per million) of CO (carbon monoxide) measured using a specific gas sensor (ToxiPro device, Biosystems, Prairieville, United States); and…”

Section: Methodsmentioning

confidence: 99%

The Influence of Passive Tobacco Exposure and Physical Exercise on Bone Tissue of Young Rats

et al. 2017

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Objective: The objective of this study is to investigate the effect of passive smoking during pregnancy and associated with swimming on bone area growth, bone mineral density (BMD), and bone mineral content (BMC). Methods: The offspring was grouped by control matrices (G1) and passive smokers (G2). The offspring was regrouped in eight subgroups, with exposure to smoking (2x/day) and physical exercise (1 session/day), respecting the group of matrices in: sedentary control (G1CS and G2CS), swimming control (G1CN and G2CN), sedentary passive smoker (G1FS and G2FS), and passive smoker swimmer (G1FN and G2FN). The area, BMD and BMC were measured by the tibia and femur and analyzed by densitometer. The results were analyzed by One-Way ANOVA test with Tukey post-test, with a significance level of 5%. Results: In the tibia BMC study, a better rate was observed in G2CN group when compared to G1CS, G1CN and G1FN (p ≤ 0.023). When assessing BMD in the femur, a higher density ratio was observed in G1FS group when compared to G2CS, G2CN, G2FS and G2FN (p<0.008). In the tibia study, the animals of the G1FS group had higher rates when compared to G2CS and G2FN groups (p≤0.007). Conclusions: The model of male offspring exposed to passive smoking during fetal development showed a strong decrease in the analyzed parameters. Level of Evidence I, Randomized High Quality Clinical Trial With or Without Statistically Significant Difference, But Narrow Confidence Intervals.

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Morphological changes in lungs, placenta, liver and kidneys of pregnant rats exposed to cigarette smoke

Cited by 41 publications

References 26 publications

Developmental cigarette smoke exposure II: Kidney proteome profile alterations in 6 month old adult offspring

Developmental cigarette smoke exposure II: Kidney proteome profile alterations in 6 month old adult offspring

Developmental cigarette smoke exposure: Kidney proteome profile alterations in low birth weight pups

The Influence of Passive Tobacco Exposure and Physical Exercise on Bone Tissue of Young Rats

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