This study was to evaluate the effect of androgen deficiency on thyroid immunoreactive C-cells and bone structure and function in a male orchidectomized middle-aged rat model. Fifteen-month-old male Wistar rats were divided into orchidectomized (Orx) and the sham-operated control (Sham) group. In the Orx group significant decreases (P < 0.05) were found in the volume of C cells (by 14%), their relative volume density (by 13%) and serum calcitonin concentration (by 54%) compared to the controls. Analyses of trabecular microarchitecture of the proximal tibia metaphysis showed that Orx induced marked decreases of cancellous bone area, trabecular thickness and trabecular number (by 52, 20 and 19% respectively; P < 0.05), whereas trabecular separation was increased by 27% (P < 0.05). In Orx rats, serum osteocalcin concentration was increased by 119% (P < 0.05), while serum calcium and phosphorus were 6 and 14% (P < 0.05) lower, respectively, compared to the levels in the Sham. In addition, urine calcium content was considerably higher (by 129%; P < 0.05) in Orx animals. These findings indicate that the androgen deficiency caused by Orx in middle-aged rats modulated the structure of C cells and diminished secretion of calcitonin. Histomorphometrical and biochemical analyses demonstrated a decrease of cancellous bone mass and increased bone turnover.
The role of membrane fluidity in determining red blood cell (RBC) deformability has been suggested by a number of studies. The present investigation evaluated alterations of RBC membrane fluidity, deformability and stability in the presence of four linear alcohols (methanol, ethanol, propanol and butanol) using ektacytometry and electron paramagnetic resonance (EPR) spectroscopy. All alcohols had a biphasic effect on deformability such that it increased then decreased with increasing concentration; the critical concentration for reversal was an inverse function of molecular size. EPR results showed biphasic changes of near-surface fluidity (i.e., increase then decrease) and a decreased fluidity of the lipid core; rank order of effectiveness was butanol > propanol > ethanol > methanol, with a significant correlation between near-surface fluidity and deformability (r = 0.697; p<0.01). The presence of alcohol enhanced the impairment of RBC deformability caused by subjecting cells to 100 Pa shear stress for 300 s, with significant differences from control being observed at higher concentrations of all four alcohols. The level of hemolysis was dependent on molecular size and concentration, whereas echinocytic shape transformation (i.e., biconcave disc to crenated morphology) was observed only for ethanol and propanol. These results are in accordance with available data obtained on model membranes. They document the presence of mechanical links between RBC deformability and near-surface membrane fluidity, chain length-dependence of the ability of alcohols to alter RBC mechanical behavior, and the biphasic response of RBC deformability and near-surface membrane fluidity to increasing alcohol concentrations.
We examined whether isoflavones increase hepatic thyroid hormone concentrations and affect cholesterol metabolism in middle-aged rats Serum T3 was not affected while hepatic T3 was almost doubled, which supports increased local T3 availability. Obtained results are compatible with displacement of TH from TTR, major transport protein in rodent blood and human CSF. Hepatic increase of T3 correlated with up-regulated expression of the Cyp7a1 gene and elevated 7α-hydroxycholesterol IF also lowered 24-hydroxycholesterol and desmosterol in liver and serum, while the total cholesterol levels remained unchanged.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.