Enzyme histochemistry of the liver in autopsy material at different post-mortem times.

The authors report the enzyme histochemistry of the liver obtained from autopsy material in 22 corpses (2 to 12 hours post-mortem) and performed to evaluate the sensitivity of enzyme activities to the autolysis process and the use of enzymes to estimate time in forensic pathology. The earliest sample was at 2 hours post-mortem; there was five cases up to 5 hours; eight case up to 8 hours and eight cases up to 12 hours since death. Active phosphorylase (PHYLA a) and total phosphorylase (PHYLA t) were negative two hours after death. PHYLA t reaction represents the activity of PHYLA a increased with the inactive phosphorylase b which can be activated by the addition of ATP and Mg2+ to the incubation medium for phosphorylase a; this activation proved to be ineffective in the post-mortem periods of this study. Glucose-6-phosphatase (G6P-A) also showed a tendency to be sensitive to the autolysis process, displaying a reaction progressively weaker or negative in the post-mortem periods of observation. The results indicate these enzymes as a possible tool to estimate time in forensic pathology deserving further investigation. Lactate dehydrogenase (L-D), alpha-glycerophosphate dehydrogenase (alpha-GP-D) and beta-hydroxybutyrate dehydrogenase (beta-HOB-D) instead showed stronger reactions as the autolysis process evolved.

Acute administration of human chorionic gonadotropin reverts some of the inhibitory effects of an LH-RH agonist on testicular steroidogenesis

An LH-RH agonist, des-Gly10, [DTrp6]-LH-RH ethylamide (LH-RH A), was administered chronically to adult male cats in order to determine its effect on the steroidogenesis of the testis during the stimulatory action of human chorionic gonadotropin (hCG). Measurement of plasma testosterone levels were combined with the histochemical analysis of some steps of the testicular steroidogenic pathway. Chronic daily treatment with LH-RH A(20 *g/kg) for 67 days inhibited the early testicular response to hCG during the initial 0.5,1 and 24 h, whereas the inhibitory egffect was not observed 48 and 72 h after hCG administration.The maximal responses to hCG were obtained both in LH-RH A-treated animals and in their control group 48 and 72 h after hCG adnministration. Under these conditions, LH-RH A-treated cats showed no alteration in 3ß-hydroxysteroid dehydrogenase (3ß-Host-D) activity, whereas a marked inhibition was observed in the activity of alcohol dehydrogenase (ADII) which reflects the activity of 20,22-desmolase and/or 17,20-desmolase.

Acute administration of human chorionic gonadotropin reverts some of the inhibitory effects of an LH-RH agonist on testicular steroidogenesis.

An LH-RH agonist, des-Gly10,[DTrp6]-LH-RH ethylamide (LH-RH A), was administered chronically to adult male cats in order to determine its effect on the steroidogenesis of the testis during the stimulatory action of human chorionic gonadotropin (hCG). Measurement of plasma testosterone levels were combined with the histochemical analysis of some steps of the testicular steroidogenic pathway. Chronic daily treatment with LH-RH A (20 micrograms/kg) for 67 days inhibited the early testicular response to hCG during the initial 0.5, 1 and 24 h, whereas the inhibitory effect was not observed 48 and 72 h after hCG administration. The maximal responses to hCG were obtained both in LH-RH A-treated animals and in their control group 48 and 72 h after hCG administration. Under these conditions, LH-RH A-treated cats showed no alteration in 3 beta-hydroxysteroid dehydrogenase (3 beta-Host-D) activity, whereas a marked inhibition was observed in the activity of alcohol dehydrogenase (ADII) which reflects the activity of 20,22-desmolase and/or 17,20-desmolase.

Histochemical and histological analysis of the Leydig cells of cats treated with a supraphysiological dose of LH-RH analog.

An LH-RH analog (des-Gly10,[D-Trp6]-LH-RH ethylamide, LH-RH A) was administered to adult male cats for 67 days (20 micrograms/kg, sc) in order to study its inhibitory effects on the structure of Leydig cells, as determined by histological and histochemical-morphometric techniques. Histological examination showed that LH-RH A promotes a decrease in the volume of the interstitial tissue. In addition, Leydig cell nuclei exhibited marked structural alterations. Morphometric analyses utilizing histochemistry of the enzyme 3-beta-hydroxysteroid dehydrogenase (3-beta-HOST-D) as a marker of Leydig cells also demonstrated a significant decrease of the relative volume occupied by the Leydig cells in the testis.

Experimental micropolycystic ovarian disease. I. Measurement of body weight, ovarian weight and histochemical activity of 17 beta-hydroxysteroid dehydrogenase.

The effects of administration of 1.25 mg testosterone propionate between the 2nd and 5th day of life on body weight, ovarian weight, food and water consumption, and the histochemical activity of 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) were studied in female Wistar rats during the evolution of experimental micropolycystic ovaries. Biometric studies showed a 9.9 day delay of vaginal opening for the treated animals and that the increased body weight of the animals during the disease was not related to food intake and thus presumably due to the induced metabolic disorder. Reduced histochemical activity of the 17 beta-HSD of testosterone-treated rats was detected at ages 30, 60 and 90 days before the onset of morphological alterations of the ovaries. The possible participation of 17 beta-HSD in the disequilibrium between androstenedione and testosterone and in the genesis of the disease is discussed.

Pós-graduaçäo em patologia humana na faculdade de medicina de Ribeiräo Preto: experiência e perspectivas / Graduation in human pathology at the Faculdade de Medicina de Ribeiräo Preto: experiences and perspectives

Após breve revisäo da legislaçäo brasileira referente à pós-graduaçäo na área médica, descreve-se a adaptaçäo dessa legislaçäo aos programas de Mestrado e Doutorado em Patologia Humana da Faculdade de Medicina de Ribeiräo Preto, bem como a experiência acumulada nos últimos 6 anos e as perspectivas desses programas

Tryptophan metabolism in alcoholic pellagra patients: measurements of urinary metabolites and histochemical studies of related muscle enzymes.

Biochemical and enzymatic aspects of tryptophan-niacin metabolism were studied in 15 adult alcoholic pellagra patients and in 14 controls. In addition to the clinical signs of niacin deficiency, most of the pellagra patients had other signs of malnutrition. Plasma tryptophan in pellagra patients was 2.07 +/- 1.27 mumol/dl, and in the controls 4.84 +/- 2.21 mumol/dl (p less than 0.001). The erythrocyte glutamic oxaloacetic transaminase index was 1.94 +/- 0.77 in the pellagra patients and 1.58 +/- 0.73 in the controls. The urinary levels of 3-hydroxyanthranilic acid were 34.49 +/- 21.47 mumol/g of creatinine in the pellagra patients and 14.51 +/- 8.02 mumol/g creatinine in the controls (p less than 0.02). The urinary levels of N'methylinicotinamide were 2.13 +/- 1.18 mg/g creatinine in the pellagra patients and 4.76 +/- 1.94 mg/g creatinine in the controls (p less than 0.01). The excretion of N'-methyl-2-pyridone-5-carboxamide (2-pyridone) was 2.94 +/- 2.37 mg/g creatinine in the pellagra patients and 10.19 +/- 7.49 mg/g creatinine in the controls (p less than 0.01). The histoenzymological activity of 3-hydroxyanthranilate oxidase in the deltoid muscle was higher in the pellagra patients than in the controls, whereas alpha-glycerophosphate dehydrogenase activity was higher in the controls. These results suggest that for alcoholic pellagra patients the tryptophan-niacin pathway is inhibited after the 3-hydroxyanthranilate oxidase step.

Apical aneurysm of Chagas's heart disease.

A retrospective study of Chagas's heart disease was carried out by a review of necropsy reports with special reference to the lesion known as the apical aneurysm. It was concluded that this lesion was more frequent in men, was unrelated to age, and was unrelated to heart weight. Patients dying of the cardiac consequences of Chagas's cardiomyopathy were more likely to have an apical aneurysm than those whose death was unrelated to the disease but the mode of death (sudden, or with heart failure) was unconnected with its presence. Transillumination from within the ventricle at necropsy was not only useful in demonstrating the aneurysm but also showed areas of myocardial thinning elsewhere. Thrombosis within the lesion was frequent. The aetiology of the apical aneurysm is discussed and it is concluded that while ischaemia, inflammation, thrombosis, and mechanical factors may produce and localise this lesion, the underlying cause is the basic pathogenetic process-parasympathetic nerve cell destruction.

A virilizing adrenal tumor with borderline elevation of urinary 17-ketosteroids and histochemical demonstration of a deficiency in the delta 5/delta 4-isomerase, 3 beta-hydroxysteroid dehydrogenase enzymatic system.

A 3-year-old girl affected by a virilizing tumor of the adrenal gland, without significant elevation in the levels of 17 ketosteroids (17-KS) urinary excretion, was studied clinically. Her symptoms started abruptyly at the age of 2, with progressive enlargement of the clitoris and the appearance of pubic hair. In various tests, the 17-KS levels barely exceeded the upper normal limits and at times remained within normal limits. The retropneumoperitoneum X-ray suggested an enlargement of the right adrenal gland and the presence of a neoplasm, which was actually discovered during surgery. Histopathological examination revealed a well-defined neoplasm, without capsule invasion and with accentuated cell polymorphism. Histoenzymology showed that the tissue lacked the enzymatic system involving 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). Indoxylesterase (I.EST-A) activity identified the tumor as originating from the internal layers of the adrenal cortex. The histochemical findings were correlated to the clinical picture and the levels of urinary 17-KS.

Enzyme histochemistry of the small intestine in inherited ichthyosis.

Enzyme histochemistry of biopsies from the small intestine of 5 patients with different forms of inherited ichthyosis and of 2 normal volunteers was performed. Two of the patients had ichthyosis vulgaris, two had non-bullous congenital ichthyosiform erythroderma and one had X-linked ichthyosis. The following enzymatic activities were examined: G6P-D, 6PG-D, NADPH2-TR, ALD-A, L-D, C-A, IC-D, S-D, M-D, NADH2-TR, ATP-AI, ATP-A II, ATP-A III, ATP-A IV, R5P-A, DHO-D, alphaGP-D, betaHOB-D, MAO, GL-D alphaGP-A I, alphaGP-A II, betaGP-A II, N.EST-A. No significant variations in the different enzymatic activities were found for the ichthyosis vulgaris and non-bullous C.I.E. cases. More pronounced variations were found in X-linked ichthyosis, with a decrease in C-A, IC-D, R5P-A, betaHOB-D, GL-D, alphaGP-A II and N.EST-A activity. Succinic dehydrogenase activity has been reported in the literature to be reduced in ichthyosis vulgaris and bullous C.I.E. However, the results obtained for our patients showed equal or higher reaction levels than in the controls.

Effect of corn and sorghum diets in N1 methylnicotinamide excretion and hepatic enzymes in rats.

This study was carried out to compare the effects of corn (Zea mays) and sorghum (Sorghum vulgare) diets on urinary N1 methylnicotinamide (N'MN) excretion and on the activity of hepatic enzyme in young adult rats. Thirty rats, weighing an average of 174.3 g at the beginning of the experiments, were divided into three groups and studied for 13 weeks. The two experimental diets supplied 7% protein, and a casein diet was used as control. Niacin was excluded from the vitamin mixture used in the corn and sorghum diets. The activities of the following enzymes were studied: betaHOB-D, G6P-D, NADH2-TR, NADPH2-TR, and 3 HOA-0. Urinary excretion of N'MN was statistically different among the three groups, the corn group having the lowest level. The corn-fed animals appeared to have more obvious alterations in liver enzyme activity. The changes found in corn and sorghum-fed animals are different and cannot be explained as due to niacin deficiency. The different amino acid compositions of the two grains and their relationship with the discrepancies in the result are also discussed.