Histoenzymatic Changes Research Articles

The influence of hollyhock extract administration on testicular function in rats

It has been reported, recently that an aqueous extract from hollyhock flowers (Althaea rosea Cav. varietas nigra) induces weak metabolic changes in rat testes. In the present study, the in vivoinfluence of a methanolic extract was investigated on the metabolism and morphology of the rat testis. To this end, histochemical, morphometric and radioimmunological methods were used. The rats drank the extract at a dose of 100 mg/day for 7 weeks. The histochemical activities of glucose-6-phosphate dehydrogenase (G6PDH) and Delta(5)beta-hydroxysteroid dehydrogenase (Delta(5)betaHSD) increased significantly statistically in the Leydig cells of the experimental rats in comparison with controls. There were no significant changes in either the diameter of seminiferous tubules or the height of seminiferous epithelium after hollyhock administration. Further, only a small amount of hyperplasia of the interstitial tissue was observed. The morphological and histoenzymatic changes in the Leydig cells indicate that the methanolic hollyhock extract has a direct but small influence on rat testes. The insignificant changes in testicular testosterone and estradiol content suggest that the extract does not disturb steroidogenesis.

Effect of epidural injection of prosidol with clonidine on the state of spinal cord and spinal ganglion.

Morphological and histoenzymatic changes in cells of the spinal cord and spinal ganglia after epidural injection of a combination of prosidol with clonidine were studied on dogs. No pathological structural and metabolic changes in the nervous tissue were found after combined treatment with the test drugs. Higher activity of nucleic acids and alkaline phosphatase in spinal neurons and spinal ganglion in experimental animals in comparison with those in controls indicates intensification of protein synthesis and active transport in the endothelium of nerve tissue capillaries, which is a favorable factor.

EFFECT OF NISOLDIPINE ON STRESS‐INDUCED MYOCARDIAL DAMAGE IN THE CONSCIOUS PIG

1. The effect of the calcium channel blocker nisoldipine on the myocardial content of lipid peroxidation products (malondialdehyde (MDA), conjugated double bonds (CDB), fluorescent end-products (RF) and mitochondrial adenine nucleotides) was investigated in conscious pigs (n = 14) subjected to 24 h of immobilization stress. Histoenzymatic and electron microscopic studies of the myocardium were also performed. Nisoldipine was given orally in a twice daily dose of 20 mg for 2 days before and on the day of the experiment. Results were compared with those obtained in immobilized untreated pigs (n = 10) and in non-stressed treated controls (n = 8). 2. Pretreatment with nisoldipine significantly attenuated stress-induced increase in myocardial contents of CDB and RF and prevented decline of mitochondrial adenine nucleotides. Stress-induced myocardial histoenzymatic changes (decrease of succinic dehydrogenase, ATPase, acid phosphatase activity) and ultrastructural alterations (mitochondrial damage, lysis of myofibrils, dilatation of sarcoplasmic reticulum and endothelial swelling) were also diminished. 3. It is concluded that treatment with a Ca2(+)-antagonist is beneficial to the heart exposed to environmental stress.

Karyometric, cytophotometric and histoenzymatic studies on neuroglia of rats treated with 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCNU/Lomoustine)

CCNU is a cytostatic drug, a nitrosourea derivative, used--among others--in therapy of tumors of the central nervous system. Even if the drug is regarded safe for central and peripheral nervous systems, a possibility of harmful effects of CCNU on the central nervous system should be examined caused by the affinity of all nitrosourea derivatives to lipids. This has prompted us to study the drug effect on neuroglia cells in corpus callosum and gyrus cinguli. The drug was administered to rats by the intragastric route in four doses--one dose a week. Three doses of 2.5 mg each were followed by one dose of 5 mg. Some brains were isolated for the studies, and paraffin sections were prepared for karyometric as well as cytophotometric studies and for section staining according to Nissl and Klüver-Barrer techniques 8 days after the last dosage. Brains of other experimental rats served for preparing cryostat sections for demonstration of phosphatase and esterase activities. The studies, conducted after CCNU administration, documented a significant decrease in size of oligodendroglia nuclei and an increase in size of astroglia nuclei. DNA content of neuroglia nuclei was markedly decreased. Histoenzymatic changes in experimental animals were not very pronounced and included a slight increase in TPPase and nonspecific esterase activities as well as a decrease in ATPase activity. Despite the changes in neuroglia cells no damage to corpus callosum myelin sheaths was observed.

Prevention of adrenaline-induced metabolic systemic and myocardial alterations by the beta-blocking agent metipranolol in the dog.

We investigated the effectiveness of the beta-blocking agent metipranolol in preventing detrimental systemic and myocardial alterations induced in healthy dogs by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Metipranolol (0.3 mg/kg) was infused intravenously concurrently with AD (1.2 micrograms/kg/min) for 4 h and blood values of free fatty acids (FFA) and triiodothyronine(T3) were measured initially, after 2 and 4 h of infusion and compared with those obtained in dogs infused with AD alone and with saline. Metipranolol suppressed a rise in free fatty acid, reversed AD-induced histoenzymatic changes in succinic dehydrogenase and ATPase activity and considerably inhibited the development of mitochondrial alterations detected in dogs infused with AD alone. A tendency to attenuate AD-induced fall in serum T3 was also detected in metipranolol-treated dogs. Results suggest that this drug might be of value in preventing consequences of increased adrenergic activity in the acute stage of myocardial infarction.

Morphology and histochemistry of the thalamus in the course of intoxication by ethyl-mercury-p-toluenesulphanilide (EMTS)

Organic Mercury compounds are known for their neurotoxicity. From our previous studies it appeared that a variable degree of damage is brought about in the individual structures of the CNS by ingestion of organic mercurials. A detailed study was undertaken on the histotopography of pathological changes occurring in the thalamus - the major integrator of various cerebral functions - following intragastric administration of EMTS, a fungicide widely applied in agriculture. Rats served as the experimental animals. They were treated intragastrically with a daily dose of 15 mg of EMTS over a period of 10 days ( the per os DL50 for rats is 100 mg/kg of body weight). The results of our study have revealed that chronic ingestion of large doses of EMTS brings about a considerable inhibition of the activities of AChE, BuTJ, acP and ATPase in many thalamic nuclei with a concomitant elevation of TPPase and NsE activities. There was considerable variation as to the degree of histoenzymatic changes in the individual thalamic nuclei. The accompanying glial reaction was evaluated aw well. An interpretation of the findings made in this study has been undertaken.

Effectiveness of insulin-glucose in preventing adrenaline-induced myocardial and systemic disturbances in the dog.

The aim of this study was to investigate whether insulin-glucose (IG) is able to prevent detrimental systemic and myocardial changes induced in healthy dog by adrenaline (AD) infused at a rate which mimics spontaneous secretion after coronary occlusion. Insulin (0.3 u/kg) and glucose (10% ml/kg) mixture was infused intravenously concurrently with AD (1.2 microgram/kg/min) for 4 h and blood values of FFA, triiodothyronine (T3) immunoreactive insulin (IRI) and glucose measured initially, after 2 and 4 h of infusion were compared with the values found in dogs infused with AD alone and with saline. IG suppressed a rise in FFA, attenuated a fall in T3, reversed AD-induced histoenzymatic changes in SDH and ATPase activity and completely prevented the development of mitochondrial alterations shown by electron microscopic study. These data provide evidence for usefulness of IG in preventing the consequences of catecholamine excess in acute stage of MI.

Histochemical and histoenzymatic changes in mouse liver in subacute benzene intoxication

The investigations were performed on mice. They were divided into a control group and 4 experimental groups. The experimental animals were administered intraperitoneally benzene 6 X every 24 h. The animals were decapitated 30 min. 4, 12 and 24 h after the last benzene administration. During the experiment, dyeing for neutral lipids and glycogen was carried out, and the activity of NADH2-r.t., SDH, G-6-Pase, ATP-ase and ACP was estimated. A decrease of glycogen content in liver cells, deviations in the amount of neutral lipids, reversible decrease of mitochondrial enzymes activity, and intensification of the processes of intracellular catabolism were found.

The dynamics of histoenzymatic changes in the kidney in acute poisoning with benzene

The experiments were carried out in mice which were divided into 4 experimental groups and a control group. In the course of the experiment SD, NADH2-tetrazolium reductase; ATP-ase, G-6-P-ase and AP were observed. It was found that acute benzene intoxication causes the disturbances in the enzymatic activities of the cells of the main segment of the nephron. The impairment of tissue respiration and oxygen phosphorylation and of active transport is due to benzene intoxication. Benzene leads to injury of the endoplasmatic reticulum in the cells of the kidney.

The influence of adrenaline secretion on the enzymes in heart muscle after acute coronary occlusion in dogs.

The influence of catecholamine secretion in the early stages of myocardial infarction upon the degree of myocardial lesions was investigated in dogs. It has been found that adrenaline release into the blood after the ligation of the coronary artery aggravates histoenzymatic changes in ventricular myocardium, manifested by the decrease in lactic and succinic dehydrogenases activity.

Contribution to the histoenzymatic changes in multiple sclerosis.

The activities of acP, alkP, ATP-ase, TPP-ase, non-specific esterase, ASS, AChE and ChE have been investigated by histochemical methods, in the brain of 2 cases of multiple sclerosis.