Alterations in the lipid composition of seminal plasma in patients with a chronic infection of the urogenital tract.

The lipid composition of seminal plasma was studied in 15 control subjects and 21 patients consulting for hypofertility and showing a chronic infection of the urogenital tract. In the infected patients a significant reduction in total cholesterol, HDL cholesterol and total phospholipids was noted. Moreover, there is a significant correlation between the rates of total cholesterol and prostatic acid phosphatases and the rates of phospholipids and proteins in seminal plasma. Knowing the role of lipids in the phenomena of maturation and capacitation of spermatozoa, such modifications enable us to understand better the functional anomalies of sperm observed in patients with chronic infection of the urogenital tract and also enable us to explain the effects of the infection on fertility.

On the glandular origin of seminal plasma lipids in man.

The aim of this study is to examine the glandular origin of seminal fluid lipids in man. The triglycerides, the total cholesterol, the non-esterified fatty acid and the total phospholipids were measured in seminal plasma of vasectomized patients (n = 8) and control subjects (n = 15). The same parameters were measured in seminal plasma collected in three fractions from split ejaculates (n = 10). The total cholesterol and the non-esterified fatty acid are principally prostatic in origin. The phospholipids are secreted by the epididymis but also by the prostate. The origin of the triglycerides seems to be very varied.

[Lipid composition of peritoneal and follicular ovulatory fluid from patients participating in an in vitro fertilization protocol]. / Etude de la composition lipidique du liquide péritonéal et folliculaire ovulatoire chez des patientes incluses dans un protocole de fécondation in vitro.

The aim of this work is to study and compare lipid composition of peritoneal and ovulatory follicular fluid of women. The studied patients are involved in a FIV protocol. We have studied 53 peritoneal fluids and 90 follicular fluids from 33 patients. On each sample the following parameters are estimated: cholesterol, triglycerides, phospholipids, non esterified fatty acids (A.G.N.E.), HDL and LDL cholesterol, HDL and LDL phospholipids. Lipid composition of follicular and peritoneal fluids differ from these of blood plasma. The two mediums studies show no differences with regard to their lipid composition. In both cholesterol is only found as HDL cholesterol. Cholesterol arising from spermatozoa membranes may be implicated in capacitation phenomenon. HDL Cholesterol, the only form found in the studied mediums, may act as a cholesterol acceptor. Theses two points partially explain the fact that follicular and peritoneal fluids are good mediums for capacitation and survival of spermatozoa.

Secretory proteins of human seminal vesicles and their relationship to lipids and sugars.

Proteins secreted by human seminal vesicles are strongly positively charged. Cellulose acetate electrophoresis show how the presence of two protein bands of vesicular origin (N3 and N4). When studied on SDS-PAGE there are three main bands of molecular weight 67, 45 and 40 kDa, respectively. These proteins may be separated by a chromatographic process using gel filtration on Sephadex G 25 M and ion exchange chromatography on CM and SP Sephadex C 50. Fructose, secreted by seminal vesicles, is excreted with specific proteins and these complexes take part to coagulum formation. During liquefaction glucose appears progressively and fructose is released from complexes with proteins. Interconversion processes that transform fructose into glucose, originate from prostatic secretion. In man, the liquefaction process seems to be not due to proteolysis, but by the way of other mechanisms that transform vesicular proteins of very high molecular weight into sub-units with lower molecular weights in the first minutes after ejaculation. In species other than man, i.e. lemurian, fructose takes part in the coagulation process with other components (albumin, ions, -SH groups). Cholesterol appears to be in relation with proteins which have high molecular weights. Half of phospholipid content of seminal plasma is probably free. Incubation of seminal plasma with spermatozoa show that these cells use triglycerides for their metabolism. The ratio between cholesterol and phospholipids is an important marker for the capacitation-decapacitation process.

Lipid composition of human seminal plasma.

This study aims at determining the amounts of cholesterol, triglycerides, phospholipids, and nonesterified fatty acids in man's seminal liquid and determining their possible variations linked with the ways of taking and congealing samples. It concludes the determinations of lipids in human seminal liquid are reproducible; the way of taking samples has no real influence; however, it seems best to centrifuge sperm immediately after liquefaction to avoid use of triglycerides and NEFA by the spermatozoa.

Histomorphometric study of the enhancement of renal compensatory hypertrophy by ACTH in the rat.

In the female adult rat, renal compensatory hypertrophy is greatly enhanced by hyperadrenocorticism elicited by the administration of ACTH given at a dose of 18 Y/100 g BW/d for 7 days after uninephrectomy (UN). This renotrophic effect of ACTH is particularly prominent in rats drinking a NaCl solution (9 g/l). In the present experiments, we performed histomorphometrical measurements of the glomerular tuft (GT) and the proximal tubule (PT) in the hypertrophying kidney (HK) remaining 7 days after UN in 10 rats treated with ACTH and 7 control animals. The histologic preparations were examined under light microscopy with the "Kontron" image analyzer. ACTH increased the weight of the HK (1213.8 +/- 20.3 mg versus 1037.3 +/- 13.3, p less than 0.001) and determined an enlargement of the cross sectional area of the GT (12559 +/- 3351.3 mu2 versus 10486 +/- 407.5, p less than 0.01) and of the epithelial area of the PT (1751 +/- 40.8 mu2 versus 1586 +/- 41.5, p less than 0.025). These morphometrical data are consistent with the increased Protein/DNA ratio - a marker of cellular hypertrophy - found in other rats studied under the same experimental conditions. The increased weight gain of the HK elicited by ACTH is related to the hypertrophy of the epithelial cells of the PT and possibly to an enlargement of the glomeruli.

[Modification of the renotrophic action of adrenal hypercorticism by nutritional factors in uninephrectomized rats]. / Modulation de l'effet rénotrophique de l'hypercorticisme surrénalien par des facteurs nutritionnels chez le rat uninéphrectomisé.

In the rat renal compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The gain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotropic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and D2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na and K by the nephron.

Enhancement of renal compensatory hypertrophy by hyperadrenocorticism and its modulation by nutritional factors.

Renal compensatory hypertrophy (RCH) is enhanced by ACTH in the uninephrectomized rat. In the present experiments, the kidney weight and its content in protein, RNA and DNA were determined in 48 adult, female rats; 24 had free access to a NaCl solution (9 g/l) and the others to a glucose solution (50 g/l). In each group 12 rats were sacrificed 2 or 7 d. after uninephrectomy (UN). In each subgroup 6 rats were treated with ACTH (18 micrograms/100 g B.W./d) from operation until autopsy. RCH has been evaluated by the arithmetical difference between the data determined in the right control kidney excised at UN and those determined in the left solitary kidney. In all the rats, hyperadrenocorticism increased significantly the weight of the solitary kidney and its content in protein and RNA. There was a significant decrease of the DNA content of the solitary kidney in the rats sacrificed 7 d. post-UN, treated with ACTH and drinking the saline solution. DNA was not affected by ACTH in the 7 other groups suggesting that ACTH favours cellular hypertrophy mainly in the rats drinking the saline solution. The renotrophic action of hyperadrenocorticism may be related to an altered handling of Na+ and K+: there was a positive correlation between the weight gain of the solitary kidney and the urinary excretion of Na+ (r = 0.507, p less than 0.001) and of K+ (r = 0.460, p less than 0.001). Hyperinsulinism was present in all the rats given ACTH; it may act as a growth factor. Hyperglycemia played an important role in former experiments but it was absent in the present studies.

Impairment of renal compensatory hypertrophy by hypothyroidism in the rat.

Renal compensatory hypertrophy (RCH) occurs in hypothyroid rate, but it is impaired when compared to RCH found in euthyroid controls. It is due to cellular hypertrophy as the DNA content does not change and the Protein/DNA ratio increases in the compensating kidney. RCH is enhanced by thyroxine (T4) with a rise in the DNA content of the compensating kidney, but the Protein/DNA ratio does not change indicating that hypertrophy is as important as hyperplasia. Corticotrophin (ACTH) given to eu and hypothyroid rats enhances RCH with an increase in the protein content of the compensating kidney without any change in its DNA content. In the hyperthyroid rats, the enhanced RCH is not further increased by ACTH and the rise in the kidney DNA content elicited by T4 is suppressed by ACTH. The Protein/DNA ratio is increased by ACTH in hypo, eu and hyperthyroid rats. The renotrophic action of ACTH is due to hyperadrenocorticism: it is related to an increased plasma testosterone level and to a disturbed Na+, K+ and glucose metabolism.

[Influence of nutritional factors on the enhancement of renal compensatory hypertrophy by hyperadrenocorticism in the rat (author's transl)]. / Modulation de l'effet rénotrophique de l'hypercorticisme surrénalien par des facteurs nutritionnels chez le rat uninéphrectomisé.

In the rat compensatory hypertrophy (RCH) was enhanced by hyperadrenocorticism induced by the administration of a long acting ACTH at a dose of 18 Y/100 g body weight/d. for 7 d. after uninephrectomy (UN). In the present experiments we compared the differences delta between the weight, the content in protein, RNA and DNA of the left solitary kidney and the same determinations done on the right kidney excised at UN 7 d. earlier. The rats drank freely a isotonic solution of NaCl (G1) or KCl (G2) or glucose (G3, G4). The rats of group G1, G2 and G3 received a standard solid food; the G4 rats ate a K poor diet. About half of the animals were treated with ACTH. RCH occurred in all the rats even when they lost body weight. The pain in weight of the solitary kidney was enhanced in all the rats treated with ACTH but not in the G2 rats loaded with KCl. This renotrophic action of hyperadrenocorticism was most prominent in the K depleted G4 rats. The protein/DNA ratio, a marker of cellular hypertrophy, was increased by hyperadrenocorticism in the G1 and G2 rats drinking respectively the NaCl or the KCl solutions. This ratio did not change in the ACTH treated G3 and G4 rats drinking the glucose solution suggesting that, in this experimental condition, cellular hyperplasia and hypertrophy occurred at the same extent. These experiments suggest that, in the uninephrectomized rat, the renotrophic action of ACTH is modulated by nutritional factors. The enhancement of RCH by ACTH may be related to hyperglycemia, hyperinsulinism or altered handling of Na+ and K+ by the nephron.

[Correlation between renal compensatory hypertrophy and urinary sodium excretion in the ACTH treated rat]. / Corrélation entre l'hypertrophie rénale compensatrice et le débit urinaire de sodium chez le rat traité par l'ACTH.

In the rat, renal compensatory hypertrophy (RCH) is enhanced by the administration of ACTH (beta 1-24 corticotrophin) given at a dose of 18 micrograms/100 g. body weight/d. after uninephrectomy. In the rats drinking tap water, the enhancement of RCH by ACTH occurs without any significant change in urinary Na+ excretion. But, in the animals drinking a NaCl solution (9 g/l), ACTH determines a polyuria with hypernatriuria and a more striking increase of RCH positively correlated with the urinary Na+ excretion.

[Free nucleotides of nerve cells, in culture]. / Nucléotides libres de cellules nerveuses en culture.

In primary cultures the free nucleotide (FN) distribution pattern showed a slight increase of adenylic nucleotides in neuroblasts as compared to glioblasts. Significant differences in the FN distribution were found between primary cultures and clonal nerve cell lines.