Biomedical subjects

G Hocman

Publications and source records attributed to G Hocman.

At least 19 recordsLinked to original sources

PubMed1994

Cetaben and fibrates both influence the activities of peroxisomal enzymes in different ways.

The effects of cetaben and clofibric acid were compared on the activities of peroxisomal enzymes in the liver and kidney of male Wistar rats. Cetaben at 200 mg/kg body wt increased the activities of all of the enzymes in the liver that were studied two to eight times, whereas the changes induced by the same dose of clofibric acid increased some of the enzymes and decreased others. In the kidney, cetaben increased the activities of all investigated peroxisomal enzymes, while clofibric acid only increased the activity of palmitoyl-CoA oxidase. The data obtained in the dose-response study of cetaben revealed a significant rise in the activities of peroxisomal enzymes in both the liver and kidney at doses of 50-100 mg/kg body wt administered over 10 days, but the maximal effect was observed at 250 mg/kg. Palmitoyl-CoA oxidase and D-amino acid oxidase respond most markedly to cetaben. Cetaben could represent an atypical peroxisomal proliferator, since it increased the activities of all peroxisomal enzymes investigated. The fact that the individual components localized in the peroxisomes do not change markedly could be of importance with respect to the function and physical properties of peroxisomes.

4-Aminobenzoic Acid↗

PubMed1994

Antimutagenic properties of fresh-water blue-green algae.

The antimutagenic properties of whole fresh-water blue-green algae Aphanisomenon flos-aquae, marketed under the commercial name "Alpha Sun" were tested using the Ames test. Simultaneous addition of both algae and Nitrovin (a mutagen) to the test medium did not reduce the mutagenic activity. On the other hand, addition of freeze-dried blue-green algae to the test medium 2-24 h before the application of mutagen reduced its mutagenic activity.

Antimutagenic Agents↗

PubMed1994

Cetaben is an exceptional type of peroxisome proliferator.

1. Cetaben in contrast to fibrates affect differently peroxisomal constituents. 2. Changes in large scale of liver non-peroxisomal parameters were compared after 10 days administration of equal doses (200 mg/kg/day) of cetaben and clofibric acid to male Wistar rats. 3. Clofibric acid treatment increased markedly the activities of FAD-glycerol-3-P dehydrogenase, beta-hydroxyacyl-CoA dehydrogenase, cytochrome-c oxidase, malic enzyme, NAD-glycerol-3-P dehydrogenase, ethoxycoumarin deethylase, p-nitroanisole demethylase and amounts of cytochrome P-450 and b5. 4. However no analogical changes were observed after cetaben treatment in the livers of experimental animals. 5. Both drugs increased the activities of alanine-glyoxylate aminotransferase-1 and acetylcarnitine transferase--enzymes with proven mitochondrial and peroxisomal location. 6. Cetaben contrary to clofibric acid does not increase solubilization of peroxisomal enzymes. 7. Enhanced acetylcarnitine transferase and alanine-glyoxylate aminotransferase-1 activities were distributed in mitochondria as well as in peroxisomes after clofibric acid treatment, however, only peroxisomes were enriched after cetaben administration. 8. The results obtained suggest that cetaben represents an exceptional type of peroxisome proliferator, specifically affecting peroxisomes, without having a negative influence on the processes of peroxisome biogenesis.

4-Aminobenzoic Acid↗

PubMed1992

Chemoprevention of cancer: protease inhibitors.

1. The defense of the organism against cancer by inhibitors of proteolytic enzymes which are able to block the metastasizing stage of the disease is reviewed. 2. The contemporary views on the possible mechanisms of the process of prevention on both molecular and cellular levels are presented.

Animals↗

PubMed1991

"Clusters" of CJD in Slovakia: the first laboratory evidence of scrapie.

Epidemic-like occurrence of Creutzfeldt-Jakob disease was observed in 1987 in Slovakia (Orava). Search for the cause of CJD focus indicated a coincidence of genetic and environmental risks in clustering patients. Since Spongiform Encephalopathies might be transmitted orally, (Bovine Spongiform Encephalopathy), the possibility of zoonotic source of CJD cases in Orava was also considered. A deficient knowledge about the occurrence of scrapie in Slovakia stimulated an examination of sheep with signs of CNS disorders in two flocks of Valasky breed in Orava. In one flock, neurohistopathological examination revealed in sheep brains lesions characteristic for scrapie. Frozen brain tissue of these animals were used for the detection of scrapie associated fibrils. They were found in 2 animals from the same flock. This is the first laboratory confirmation of scrapie in Czecho-Slovakia. The possible epidemiological and economical implications are emphasized.

Animals↗

PubMed1989

Prevention of cancer: vegetables and plants.

1. Results of epidemiological studies indicate that a human diet rich in vegetables may lower the incidence of cancer. 2. This preventive effect of the vegetable diet against cancer could be ascribed to lowered intake of energy (joules) and its content of vitamins and carotene. 3. The consumption of vegetables means also less meat and fats as well as increased fiber content and specific chemopreventive compounds (indoles, plant phenols) present in such a diet. 4. The supposed mechanisms of prevention may include enhanced enzymatic detoxification of harmful compounds, and inhibition of their binding to cellular DNA, their adsorption on fiber, detoxification of radical forms of carcinogens by natural antioxidants in plants and probably many other ways too.

Diet↗

PubMed1988

Chemoprevention of cancer: phenolic antioxidants (BHT, BHA).

1. The synthetic phenolic antioxidants (e.g. BHT, BHA) added to human and animal food are able to lengthen the life of organisms and lower the incidence of cancer caused by chemical compounds. 2. On the other hand they may not be rendered completely harmless since they can cause lung damage (BHT) or promote the action of some carcinogens (BHA). 3. They could act as compounds preventing cancer either via interception of harmful free radicals, activating the detoxifying enzymes of the body, inhibiting the formation of ultimately carcinogenic metabolites and their binding to DNA, and modifying the immune response of the organism. 4. Their action is influenced by their own chemical structure, the composition of carcinogen, the strain, sex and age of experimental animals, the tissue upon which they are supposed to act and the time of their administration in relation to the time of the carcinogen insult. 5. These compounds are concentrated in adipose tissue, liver and kidney. They are excreted within tens of hours mainly in urine. 6. The acceptable daily intake of BHA is at present considered to be 0.6 mg kg-1 body wt day-1. In spite of their possible tumor-promoting properties they could not be considered overtly toxic. Their pronounced chemoprotective role against some forms of chemical carcinogenesis deserves considerable attention.

Animals↗

PubMed1988

Chemoprevention of cancer: selenium.

1. Selenium intake (in the form of selenite, selenate, selenomethionine, etc.) protects the organism against the action of some kinds of carcinogens. 2. People and animals having less Se in their blood are at a higher risk of acquiring cancer than those whose blood contains more of this element. 3. This chemopreventive action is probably due to antioxidant properties of Se, its involvements in the enzyme glutathione peroxidase as well as in the inhibition of enzymes converting carcinogens to their ultimate forms in the cell. 4. An intake of 150-300 micrograms of Se daily is considered to be adequate to protect the human organism without exhibiting the toxic properties of this element.

Animals↗

PubMed1988

Prevention of cancer: restriction of nutritional energy intake (joules).

1. The reduction of nutritional energy intake (joules) often reduces the incidence of both spontaneous and induced cancers in humans and experimental animals in an approximately dose-dependent manner. 2. To achieve the best preventive effect, the reduction of dietary intake should begin well before the carcinogen insult, should be intense enough (lowering the intake of joules by at least approx. 25-30%) and should last a long time, preferably even life-long. 3. This preventive effect depends upon the strain, sex and age of animals, the kind of carcinogenic insult and also the susceptibility of the target tissue. 4. The mechanism by which the dietary restriction may exert its protective action may involve changes in the hormonal equilibria, influences upon the immuno-surveillance, changes of activities of enzymes involved in carcinogen metabolism and other factors. 5. Since over-eating and the resulting obesity constitutes a pronounced risk factor for the incidence of cancer and other diseases, lowering the nutritional energy intake represents today the simplest, cheapest and most effective way to prevent cancer in the general population.

Animals↗

PubMed1981