scholarly journals Particle Deposition in Spontaneously Hypertensive Rats Exposed via Whole-Body Inhalation: Measured and Estimated Dose

2006 ◽  
Vol 93 (2) ◽  
pp. 400-410 ◽  
Author(s):  
Lindsay B. Wichers ◽  
William H. Rowan ◽  
Julianne P. Nolan ◽  
Allen D. Ledbetter ◽  
John K. McGee ◽  
...  
1994 ◽  
Vol 71 (4) ◽  
pp. 583-603 ◽  
Author(s):  
Yvonne V. Yuan ◽  
David D. Kitts

The effects of dietary protein on Ca bioavailability and utilization in bone were examined in male spontaneously hypertensive rats (SHR) fed on diets containing either casein (200 g/kg (control), 60 g/kg or heat-damaged (HD) 200 g/kg) or soya-bean protein isolate (200 g/kg (control), 60 g/kg, or HD 200 g/kg). Casein was heat-damaged to limit caseinophosphopeptide (CPP) production in order to evaluate casein enhancement of Ca bioavailability. All diets contained an adequate level of Ca (5 g/kg). A 24 h mineral balance study was performed when animals were 10 weeks old, followed by measurement of in situ paracellular Ca disappearance, femur mineralization and biomechanics at 14 weeks of age. Digestibility of soya-bean and both HD proteins estimated in vitro was reduced compared with native casein. Animals fed on HD and 60 g/kg protein diets exhibited decreased (P < 0.05) body weight gain, dry matter intake and feed efficiency compared with controls. The ileal disappearance of 45Ca was lower (P < 0.05) in animals fed on HD casein and all the soya-bean protein diets. Ca balance was not strongly affected by dietary treatments. A significant (P < 0.05) interaction between protein source and reduced protein intake was observed for femur calcification and physical measurements. Femur bending failure energy and biomechanical force measurements were reduced (P < 0.05) in HD and 60 g/kg casein and soya-bean protein fed animals. These findings suggest that whole-body Ca homeostatic mechanisms were involved in compensating for reduced Ca bioavailability and retention from casein diets modified to reduce protein digestibility and CPP production.


1980 ◽  
Vol 21 (4) ◽  
pp. 602-602
Author(s):  
Jin Yamamoto ◽  
Nick C. Trippodo ◽  
Edward D. Frohlich

2012 ◽  
Vol 302 (2) ◽  
pp. R274-R282 ◽  
Author(s):  
Kanchan Bhatia ◽  
Ahmed A. Elmarakby ◽  
Azza El-Remessey ◽  
Jennifer C. Sullivan

NADPH oxidase has been implicated in ANG II-induced oxidative stress and hypertension in males; however, the contribution of oxidative stress to ANG II hypertension in females is unknown. In the present study, we tested the hypothesis that greater antioxidant capacity in female spontaneously hypertensive rats (SHR) blunts ANG II-induced oxidative stress and hypertension relative to males. Whole body and renal cortical oxidative stress levels were assessed in female and male SHR left untreated or following 2 wk of chronic ANG II infusion. Chronic ANG II infusion increased NADPH oxidase enzymatic activity in the renal cortex of both sexes; however, this increase only reached significance in female SHR. In contrast, male SHR demonstrated a greater increase in all measurements of reactive oxygen species production in response to chronic ANG II infusion. ANG II infusion increased plasma superoxide dismutase activity only in female SHR (76 ± 9 vs. 190 ± 7 Units·ml−1·mg−1, P < 0.05); however, cortical antioxidant capacity was unchanged by ANG II in either sex. To assess the functional implication of alterations in NADPH enzymatic activity and oxidative stress levels following ANG II infusion, additional experiments assessed the ability of the in vivo antioxidant apocynin to modulate ANG II hypertension. Apocynin significantly blunted ANG II hypertension in male SHR (174 ± 2 vs. 151 ± 1 mmHg, P < 0.05), with no effect in females (160 ± 11 vs. 163 ± 10 mmHg). These data suggest that ANG II hypertension in male SHR is more dependent on increases in oxidative stress than in female SHR.


2007 ◽  
Vol 292 (2) ◽  
pp. R764-R768 ◽  
Author(s):  
Jennifer C. Sullivan ◽  
Jennifer M. Sasser ◽  
Jennifer S. Pollock

Male spontaneously hypertensive rats (SHR) have a blunted pressure-natriuresis relationship and enhanced oxidative stress compared with female SHR. Furthermore, oxidative stress contributes to abnormal renal Na+ handling and renal damage in hypertension. The aim of this study was to determine whether a sex difference exists in renal inner medullary hydrogen peroxide (H2O2) levels and/or antioxidant systems in SHR and the influence of sex steroids on these systems. Thirteen-week-old intact and gonadectomized male and female SHR were placed in metabolic cages for 24-h urine collection. Renal inner medullas were isolated for antioxidant activity assays and Western blot analysis or for measurements of H2O2 using Amplex Red. Studies verified that male SHR had greater Na+ reabsorption compared with female SHR. Male SHR had enhanced urinary excretion of H2O2 compared with female SHR. Gonadectomy decreased H2O2 excretion in males and increased H2O2 excretion in females, suggesting that testosterone stimulates total body oxidative stress and estrogen suppresses levels of total body oxidative stress. There was not a sex difference in inner medullary H2O2 levels. Male SHR had a testosterone-dependent increase in inner medullary SOD activity, and both intact and gonadectomized males had high levels of inner medullary catalase activity compared with females. The results of this study showed that there was a sexual dimorphism in Na+ handling and oxidant status. We hypothesize that there is a testosterone-sensitive increase in whole body reactive oxygen species production that results in a compensatory increase in the inner medullary antioxidant capability possibly to normalize Na+ handling.


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