ABSTRACT
In animals, long-term feeding with peanut (Arachis hypogaea) seed coats causes hypertrophy and hyperplasia of the thyroid gland. However, to date there have been no detailed studies. Here, we explored the thyroidal effects of dietary peanut seed coats (PSC) in rats. The PSC has high levels of pro-goitrogenic substances including phenolic and other cyanogenic constituents. The PSC was mixed with a standard diet and fed to rats for 30 and 60 days, respectively. Animals fed with the PSC-supplemented diet showed a significant increase in urinary excretion of thiocyanate and iodine, thyroid enlargement, and hypertrophy and/or hyperplasia of thyroid follicles. In addition, there was inhibition of thyroid peroxidase (TPO) activity, 5’-deiodinase-I (DIO1) activity, and (Na+-K+)-ATPase activity in the experimental groups of rats as compared to controls. Furthermore, the PSC fed animals exhibited decreased serum circulating total T4 and T3 levels, severe in the group treated for longer duration. These data indicate that PSC could be a novel disruptor of thyroid function, due to synergistic actions of phenolic as well as cyanogenic constituents.
Subject(s)
Animal Feed/adverse effects , Animals , Antithyroid Agents/isolation & purification , Antithyroid Agents/toxicity , Arachis/chemistry , Drug Synergism , Glucosides/analysis , Glucosides/pharmacology , Glucosides/toxicity , Hyperplasia , Hypertrophy , Hyperthyroidism/blood , Hyperthyroidism/chemically induced , Iodide Peroxidase/antagonists & inhibitors , Iodine/urine , Male , Nitriles/analysis , Nitriles/pharmacology , Nitriles/toxicity , Ovule/chemistry , Polyphenols/analysis , Polyphenols/pharmacology , Polyphenols/toxicity , Rats , Rats, Wistar , Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors , Thiocyanates/urine , Thyroid Gland/drug effects , Thyroid Gland/enzymology , Thyroid Gland/pathology , Thyroid Hormones/bloodABSTRACT
Aim: The effect of crude extract of apple on the activity of Na+/K+-ATPase in the liver, kidney and heart tissues of rats was investigated. Methodology: Two separate test groups of animals were fed a standard laboratory diet, water and given 1 ml and 1.5 ml/ kg body weight of crude extract of apple respectively. The control animals were fed the diet and water. The animals were treated for 6 weeks and then sacrificed. The liver, kidney and heart were excised from the rats and subsequently used for analysis of Na+/K+-ATPase. Results: The results obtained indicate that there was no significant (p>0.05) change in body weights of rats administered 1 ml and 1.5 ml/ kg body weight of apple extract. Similarly no significant (P>0.05) change was observed in the weight of liver, kidney and heart of test rats relative to control. Examination of the data reveal that the activity of the enzyme was significantly (P<0.05) decreased in the kidney but not in the liver and heart of the rats treated with the extract as compared to control. The renal Na+/K+-ATPase activity was lowest in rats treated with an extract dose of 1.5 ml / kg body weight of extract. Conclusion: The present study has shown that the Na+/K+-ATPase activity in the kidney was inhibited by apple extract. The inhibition of the enzyme is suspected to be due to some phytochemicals present in apple. However, this suggestion remains to be scientifically confirmed.
ABSTRACT
Objectives: Fenproporex is an amphetamine-based anorectic which is rapidly converted into amphetamine in vivo. Na+, K+-ATPase is a membrane-bound enzyme necessary to maintain neuronal excitability. Considering that the effects of fenproporex on brain metabolism are poorly known and that Na+, K+-ATPase is essential for normal brain function, this study sought to evaluate the effect of this drug on Na+, K+-ATPase activity in the hippocampus, hypothalamus, prefrontal cortex, and striatum of young rats. Methods: Young male Wistar rats received a single injection of fenproporex (6.25, 12.5, or 25 mg/kg intraperitoneally) or polysorbate 80 (control group). Two hours after the last injection, the rats were killed by decapitation and the brain was removed for evaluation of Na+, K+-ATPase activity. Results: Fenproporex decreased Na+, K+-ATPase activity in the striatum of young rats at doses of 6.25, 12.5, and 25 mg/kg and increased enzyme activity in the hypothalamus at the same doses. Na+, K+-ATPase activity was not affected in the hippocampus or prefrontal cortex. Conclusion: Fenproporex administration decreased Na+, K+-ATPase activity in the striatum even in low doses. However, in the hypothalamus, Na+, K+-ATPase activity was increased. Changes in this enzyme might be the result of the effects of fenproporex on neuronal excitability. .
Subject(s)
Animals , Male , Amphetamines/administration & dosage , Brain/drug effects , Brain/enzymology , Sodium-Potassium-Exchanging ATPase/metabolism , Injections, Intraperitoneal , Rats, Wistar , Time FactorsABSTRACT
PURPOSE: Na+-K+ ATPase Activity has beem estimated by the degree of inhibition of cation transport by cardiac glycosides (ouabain) using Rb-86 as a substrate. The biological characterist-Isc of T1-201 is known to be simiIar to those of potassium as a transport substrate in the presence of glucose, insulin or phobol myristate acetate (PMA). The purpose of this study was to measure ouabain sensitive Na+-K+ ATPase activity using T1-201 and compare with that using Rb-86. MATERIALS AND METHODS: Smooth muscle cells isolated from rat aorta or human placental umbilical artery were cultured, and used to measure cellular Na+-K+ ATPase activity. Na+-K+ ATPase activity was measured as a percentage decrease in cellular uptake of T1-201 or Rb-86 by ouabain under the presence of glucose, insulin or PMA in media. RESULTS: Na+-K+ ATPase ase activity measured with T1-201, as a transport substrate, was not different from those measured with Rb-86 in rat or human smooth muscle cell preparation. Incubation with high concentration glucose resulted in about 30% decrease in enzyme activity. In contrast, insulin or PMA resulted in 50-70% or 28% increases from baseline activity, respectively. CONCLUSION: These results suggests that T1-201 could replace Rb-86 in measurement of ouabain sensititive Na+-K+ ATPase activity in vitro. High level of glucose concentration decreased cellular Na+-K+ ATPase activity, but insulin or PMA increased it.
Subject(s)
Animals , Humans , Rats , Adenosine Triphosphatases , Aorta , Cardiac Glycosides , Glucose , Insulin , Membranes , Myocytes, Smooth Muscle , Myristic Acid , Ouabain , Potassium , Umbilical ArteriesABSTRACT
The effect of an organic peroxide, t-butylhydroperoxide (t-BHP), on glutamate uptake was studied in synaptosomes prepared from cerebral cortex. t-BHP inhibited the Na+/-dependent glutamate uptake with no change in the Na+/-independent uptake. This effect of t-BHP was not altered by addition of Ca2+ channel blockers (verapamil, diltiazem and nifedipine) or PLA2 inhibitors (dibucaine, butacaine and quinacrine). However, the effect was prevented by iron chelators (deferoxamine and phenanthroline) and phenolic antioxidants (N,N'-diphenyl-phenylenediamine, butylated hydroxyanisole, and butylated hydroxytoluene). At low concentrations (< 1.0 mM), t-BHP inhibited glutamate uptake without altering lipid peroxidation. Moreover, a large increase in lipid peroxidation by ascorbate/Fe2+ was not accompanied by an inhibition of glutamate uptake. The impairment of glutamate uptake by t-BHP was not intimately related to the change in Na+/-K+/-ATPase activity. These results suggest that inhibition of glutamate uptake by t-BHP is not totally mediated by peroxidation of membrane lipid, but is associated with direct interactions of glutamate transport proteins with t-BHP metabolites. The Ca2+ influx through Ca2+ channel or PLA2 activation may not be involved in the t-BHP inhibition of glutamate transport.
Subject(s)
Antioxidants , Brain , Butylated Hydroxyanisole , Carrier Proteins , Cerebral Cortex , Chelating Agents , Diltiazem , Glutamic Acid , Iron , Lipid Peroxidation , Membranes , Phenol , Synaptosomes , tert-ButylhydroperoxideABSTRACT
Na+-K+-ATPase activity of the erythrocyte plasma membrane in noninsulin-de- pendent diabetes mellitus (NIDDM) was studied together with the red cell deform-ability (RCD) and other influencing factors. Comparing with the normal controls, Na+-K+-ATPase activity, Mg++-ATPase activity, and RCD in diabetics were significantly decreased, and the erythrocyte membrane cholesterol and lipid peroxide, fasting blood glucose, and glycosylated hemoglobin were significantly increased. The change of Na+-K+-ATPase activity was positively correlated with RCD, and inversely correlated with fasting blood glucose, erythrocyte membrane cholesterol, and lipid peroxide. The results suggested that the change of Na+-K+-ATPase activity in erythrocyte may contribute to the alterations of RCD in diabetics
ABSTRACT
Objective To study the effects of chronic ouabain treatment on Na+-K+-ATPase activity and the expression of dopamine D1 receptor in rat kidney cortex. Methods A total of 28 male Sprague-Dawley (SD) rats were randomly divided into ouabain group and control group,which were treated with ouabain or saline for 5 weeks; rat tail systolic blood pressure (SBP) was recorded weekly. Rats were sacrificed after 3 and 5 weeks,respectively. Then Na+-K+-ATPase activity and the expression of dopamine D1 receptor in rat kidney cortex were measured by colorimetric assay and real-time PCR,respectively. Results After 3 weeks of ouabain treatment,the mean SBP did not change significantly,but the Na+-K+-ATPase activity increased (P