Effect of fetal exposure to gentamicin on phosphate transport in young rat kidney

1993 ◽  
Vol 265 (6) ◽  
pp. F807-F812
Author(s):  
M. Lelievre-Pegorier ◽  
S. Euzet ◽  
C. Merlet-Benichou

The renal phosphate (Pi)-transporting capacity normally increases, due to increased carrier system affinity, during the third postnatal week in rats. However, the tubular Pi reabsorption of rat pups born from gentamicin-treated mothers does not increase during this period. This study determines whether exposure to gentamicin in utero selectively alters the postnatal maturation of the carrier affinity for Pi. Pi and glucose transports by proximal tubule brush-border membrane (BBM) were studied. The maximal rate of uptake (Vmax) of Na-Pi cotransport was significantly lower (536 +/- 169 pmol.mg protein-1.10 s-1; n = 6, P < 0.01) in gentamicin-exposed rats than in controls (1,021 +/- 167 pmol.mg protein-1.10 s-1, n = 6), whereas the Michaelis constant (Km) values were the same. Gentamicin exposure had no effect on plasma parathyroid hormone concentration or on BBM glucose transport activity. The total phospholipid content of BBM, their phospholipid composition, cholesterol content, and cholesterol-to-total phospholipid mole ratio were unaltered, suggesting that membrane fluidity was unchanged. The Vmax of BBM alkaline phosphatase was lower in gentamicin-exposed rats than in controls.

1983 ◽  
Vol 245 (3) ◽  
pp. C241-C247 ◽  
Author(s):  
G. N. Pierce ◽  
N. S. Dhalla

Heart sarcolemmal membranes were isolated by the hypotonic shock-LiBr treatment from rats with chronic diabetes induced by a streptozotocin (65 mg/kg, iv) injection. Sarcolemmal Mg2+-dependent ATPase activity was elevated, whereas 5'-nucleotidase and K+-p-nitrophenylphosphatase activities in diabetic heart were depressed in comparison to control preparations. Although patent Na+-K+-ATPase and patent ouabain-sensitive Na+-K+-ATPase activities were unaltered, latent Na+-K+-ATPase activities, as determined in membranes after alamethicin or deoxycholate treatments, were found to be significantly depressed in diabetic animals. A depression in the latent Na+-K+-ATPase activity in diabetic preparations was also observed in membranes prepared by the sucrose density gradient method. Insulin-treated diabetic rats were observed to have normalized latent Na+-K+-ATPase activities. Total phospholipid content did not differ, but cholesterol content of the sarcolemmal membranes was significantly increased in diabetic heart preparations. Sarcolemmal Na+-K+-ATPase activity in diabetic heart was more resistant to treatments with filipin, an agent known to bind with cholesterol residues. These results suggest that chronic experimental diabetes is associated with some defects in sarcolemmal enzymatic activities and composition.


1987 ◽  
Vol 252 (3) ◽  
pp. E375-E379 ◽  
Author(s):  
M. Kubo ◽  
K. Y. Hostetler

Diethylaminoethoxyhexestrol caused a foam cell lipidosis in humans characterized by phospholipid storage in the liver, spleen, and other tissues, and this represents the first description of acquired lipidosis caused by a drug. It has been proposed that diethylaminoethoxyhexestrol causes phospholipid fatty liver by concentrating in lysosomes and inhibiting phospholipases but it has not previously been possible to measure the intralysosomal concentration of diethylaminoethoxyhexestrol. In this paper we report for the first time the intralysosomal concentration of this drug in rats. After a single oral dose of diethylaminoethoxyhexestrol (100 mg/kg) the intralysosomal concentration was 7.9 mM at 2.5 h, 15.6 mM at 12 h, and 20.9 mM at 24 h, respectively. The total phospholipid content of lysosomes in drug-treated rats increased 1.9-, 6.0-, and 7.6-fold over control at 2.5, 12, and 24 h, respectively. Purified lysosomal phospholipase A1 was strongly inhibited by diethylaminoethoxyhexestrol in vitro. In phospholipid fatty liver, phospholipid accumulation in lysosomes appears to be caused by the presence of diethylaminoethoxyhexestrol in lysosomes at concentrations estimated to be 7.9–20 mM, because drug levels above 1 mM completely block the activity of purified lysosomal phospholipase A1 in vitro.


1964 ◽  
Vol 42 (8) ◽  
pp. 1183-1194 ◽  
Author(s):  
J. Blumenstein

An attempt was made to produce 'forced methylation' and subsequent reduction of lecithin content of livers of rats fed a semipurified diet. The addition of guanidoacetic acid to the diet of the rats did not alter either the total phospholipid extracted from their livers or the liver lecithin content significantly. This constant pattern was observed whether choline was included in the diet or not. However, in animals fed a diet deficient in choline, the ratio of lecithin and cephalin extracted from their livers was altered, although the total phospholipid content remained constant.


1967 ◽  
Vol 20 (6) ◽  
pp. 1205 ◽  
Author(s):  
PJ Quinn ◽  
IG White

The concentration of total phospholipid, phosphatidylcholine, phosphatidylethanolamine, and choline plasmalogen in spermatozoa from the caput epididymis of the ram was higher than in spermatozoa from the cauda. The phospholipid composition of spermatozoa from the latter region of the epididymis more closely resembled ejaculated spermatozoa.


2007 ◽  
Vol 98 (5) ◽  
pp. 984-990 ◽  
Author(s):  
Samina Salim ◽  
Neelam Farooq ◽  
Shubha Priyamvada ◽  
Mohammad Asghar ◽  
Syed Jalal Khundmiri ◽  
...  

Ramadan fasting is a unique model of fasting in which Muslims the world over abstain from food and water from dawn to sunset for 1 month. We hypothesized that this model of prolonged intermittent fasting would result in specific adaptive alterations in rat kidney to keep a positive balance of metabolites and inorganic phosphate (Pi). The effect of Ramadan-type fasting was studied on enzymes of carbohydrate metabolism and brush border membrane (BBM) and BBM uptake of 32Pi in different renal tissue zones in the rat model. Rats were fasted (12 h) and then re-fed (12 h) daily for 30 d similar to human Ramadan fasting. Ramadan-type fasting resulted in increased serum Pi and phospholipids, whereas Pi clearance decreased. Serum creatinine and its clearance were not affected. Fasting caused a significant decrease in the activities of lactate and malate dehydrogenases, glucose-6-phosphatase and fructose-1,6-bisphosphatase, both in the renal cortex and medulla. However, the activity of glucose-6-phosphate dehydrogenase profoundly increased but that of malic enzyme decreased. The activities of alkaline phosphatase and γ-glutamyl transpeptidase in BBM decreased, whereas transport of 32Pi significantly increased. The decrease in enzyme activities and increase in 32Pi transport were due to alterations of both maximal velocities and relative affinities. The results indicate that Ramadan-type fasting caused specific metabolic alterations with enhanced Pi conservation in different kidney tissues in a rat model used for Ramadan fasting in man.


1958 ◽  
Vol 25 (2) ◽  
pp. 202-214 ◽  
Author(s):  
A. K. R. McDowell

Samples of milk, skim-milk and raw cream from one factory and of pasteurized cream, buttermilk and butter from two factories were taken twice monthly for varying periods for estimation of total phospholipids and (in butter only) of lecithin, cephalin and sphingomyelin.Seasonal variations in the phospholipid contents of milk, skim-milk and raw cream over 13 months probably were due to the greater proportion of small fat globules in autumn (late lactation) milk compared with spring (early lactation) milk.There were regularly recurring seasonal variations in total phospholipid content of the butters over 3 years. Maximum results were found during autumn and minimum results in winter. Lecithin, cephalin and sphingomyelin contents followed the same trends as the total phospholipid contents.Seasonal variations in phospholipid contents of buttermilks and butters were due mainly to variations in the amount of phospholipid per unit of fat in the cream. Differences in butter-making technique had little effect on the proportion of phospholipids from the cream retained in the butter.Average results for total phospholipid content of the products examined were: milk, 0·038% (0·031–0·050%); skim-milk, 0·018% (0·014–0·023%); buttermilk, 0·156% (0·103–0·191%); butter, 0·133% (0·099–0·181%). The average result for percentage of total phospholipid in the fat of the raw creams examined was 0·44% (0·38–0·51%); and in the fat of the pasteurized creams 0·41% (0·35–0·49%). Average weighted results for total phospholipid and for lecithin, cephalin and sphingomyelin contents of butter were 0·139, 0·041, 0·051 and 0·047% respectively.


1980 ◽  
Vol 26 (2) ◽  
pp. 232-234 ◽  
Author(s):  
E J van Voorst tot Voorst

Abstract The total phospholipid content of the supernatant fluid decreases rapidly with increasing relative centrifugal force when amniotic fluid is centrifuged. Possible explanations for this are discussed. The effect of storage on the total phospholipid content of amniotic fluid at different temperatures and the influence of contamination with blood and meconium are also described.


1982 ◽  
Vol 242 (6) ◽  
pp. E378-E383 ◽  
Author(s):  
J. Ruel ◽  
P. Coulombe ◽  
J. H. Dussault

We studied the effects of thyroid hormones and malnutrition on protein, DNA, and phospholipid content of the developing rat lung during the first month of life. Neonatal hypothyroidism significantly decreases the lung phospholipid content by 30-45% between 5 and 30 days of age whether the results are expressed per milligram DNA or per gram tissue. Administration of thyroxine for 3 days to hypothyroid rats increases significantly (20%) their total phospholipid content, mainly through its preferential effect on phosphatidylcholine (50% increase). Adult animal response to thyroid hormones is markedly different from that observed in young rats for most parameters examined. In malnourished rats, lung tissue phospholipids are decreased per cell but not per unit cell mass after 11 days of age. These results show that hypothyroidism has a specific effect on lung phospholipids during the neonatal period.


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