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Biomedical subjects

F Böhm

Publications and source records attributed to F Böhm.

At least 19 recordsLinked to original sources
PubMed2001

Dietary uptake of lycopene protects human cells from singlet oxygen and nitrogen dioxide - ROS components from cigarette smoke.

There is current interest in the health benefits of dietary carotenoids and the possible deleterious effects on certain sub-populations such as smokers. Here we report in vivo protection of human lymphocytes, conferred by dietary supplementation of lycopene rich foods against the reactive oxygen species, NO(2)(*) radical (by electron transfer) and 1(O)(2) (by energy transfer). It was found that a lycopene rich diet, maintained for 14 days, increased the serum lycopene level 10 fold compared to serum obtained after the same period, where a typical western European diet had been consumed. Relative lymphocyte protection factors of 17.6 and 6.3 against NO(2)(*) radical and 1(O)(2), respectively, were obtained, which re-enforce epidemiological data, showing protection against several chronic diseases by tomato lycopene.

Antioxidants↗
PubMed2000

Enhanced vasoconstrictor response to endothelin-B-receptor stimulation in patients with atherosclerosis.

The vascular responses to endothelin-1 [ET-1; nonselective endothelin-A and -B (ET(A) and ET(B) agonist)] and sarafotoxin 6c (S6c; ET(B) agonist) were investigated in patients with atherosclerosis. ET-1 and S6c (3, 10 and 30 pmol/min) were infused into the brachial artery while forearm blood flow (FBF) was measured by venous occlusion plethysmography in seven male patients with atherosclerosis and six age-matched healthy male controls. S6c evoked an initial increase followed by a dose-dependent reduction in FBF. The initial dilator component did not differ between the two groups. The vasoconstrictor component of the two lower doses of S6c was significantly larger in the atherosclerotic patients than in controls. The reduction in FBF induced by 3 and 10 pmol/min S6c was 18 +/- 2% and 27 +/- 6% in the control group compared to 29 +/- 3% (p < 0.02) and 42 +/- 2% (p < 0.05) in patients with atherosclerosis. The vasoconstrictor response to S6c correlated with low-density lipoprotein (LDL) cholesterol levels (r = 0.47, p < 0.05). The vasoconstrictor response to ET-1 was similar in the two groups. It is concluded that the forearm vasoconstrictor response to S6c but not that to ET-1 is enhanced in patients with atherosclerosis as compared with healthy controls. This finding suggests an upregulation of vascular smooth muscle ET(B)-receptors in atherosclerosis.

Aged↗
PubMed1999

[Round window membrane defect in divers].

BACKGROUND: The rupture of the round window membrane is a special form of traumatic inner ear deafness. Because of the changing pressure levels, divers are at risk of developing such a membrane rupture, especially if tube function is disturbed. As the popularity of diving as a sport increases, ENT specialists have to deal with diving related problems increasingly frequently. PATIENTS AND METHODS: Seven cases of divers are presented in whom a tympanotomy was performed following the diagnosis of a rupture of the round window membrane. The symptoms and intraoperative findings are discussed and the otologic and diving literature is reviewed. Following a case report, the pathophysiology, clinical symptoms and differential diagnosis of round window ruptures are discussed controversially. Possible therapeutical consequences are described. RESULTS: None of our patients exhibited the classical triad of deafness, tinnitus, and vertigo as described in the diving literature. The leading symptom in our patients was the loss of hearing; only two patients had vertigo. Tinnitus was found in half of the patients. Intraoperative a rupture of the round window membrane was presumed in five divers. CONCLUSIONS: If disturbance of inner ear function does occur concurrently with diving, a rupture of the round window membrane must be considered. An otologic examination must be performed in any diver with a loss of hearing and/or signs of a barotrauma of the middle ear. After differential diagnosis to exclude other possibilities, a tympanotomy to cover the round window membrane should be performed if symptoms persist more than 24 hours.

Adult↗
PubMed1998

Beta-carotene with vitamins E and C offers synergistic cell protection against NOx.

The peroxynitrite anion and the nitrogen dioxide (radical) are important toxic species which can arise in vivo from nitric oxide. Both in vivo and in vitro cell protection is demonstrated for beta-carotene in the presence of vitamin E and vitamin C. A synergistic protection is observed compared to the individual anti-oxidants and this is explained in terms of an electron transfer reaction in which the beta-carotene radical is repaired by vitamin C.

Antioxidants↗
PubMed1998

Enhanced protection of human cells against ultraviolet light by antioxidant combinations involving dietary carotenoids.

Antioxidants like beta-carotene, alpha-tocopherol and ascorbic acid should be able to protect human cells against damage due to ultraviolet light. Cultured human fibroblasts have been irradiated with UVA or UVB light after incubation with the antioxidants or combinations of them. The efficiency of the protection by the antioxidants in dietary concentrations is estimated by cell counting following cell culture. In the case of UVA irradiation we find synergistic effects of combinations with beta-carotene as the main protector. On the other hand, only additive effects of the tested combinations are observed in the experiments with UVB light. Our experiments show a protective effect of dietary antioxidants against human tissue cell damage by ultraviolet light.

Antioxidants↗
PubMed1997

Different DNA repair time courses in human lymphoid cells after UVA, UVA1, UVB and PUVA in vitro.

The time course of DNA repair was investigated using the nucleoid sedimentation technique. Human lymphoid cells were irradiated with membrane related equitoxic doses of UVB, UVA/B, UVA and UVA1. Additionally, PUVA treatment of cells using two different light sources was performed. It was found that in the case of UVB and UVA/B irradiation of the cells, DNA repair activity arose lasting not longer than 4 h. However, in the case of UVA and UVA1 no repair activity was detectable with the used method but an increasing nucleoid density believed to indicate apoptosis. This could be shown with the same irradiation protocol. When the irradiation dose of UVA and UVA1 was lowered to one fifth of the equitoxic dose neither repair activity nor apoptosis was detected. There was no difference between UVA and UVA1 with respect to the nucleoid density time course. Hence, the initial absorbing chromophore is probably located in the UVA1 region. In the case of PUVA, we found DNA repair that was complete after 12 h. The UVB part in the irradiation spectrum of a PUVA system had an accelerating effect on the repair kinetics. The time course of DNA density appears to be related to subsequent cell behaviour: apoptosis or incomplete DNA repair including the risk of mutation.

DNA Repair↗
PubMed1995

Bilirubin phototoxicity to human cells by green light phototherapy in vitro.

Phototherapy of newborn infants with blue or green light is the most common treatment of neonatal hyperbilirubinemia. Using bilirubin bound to human lymphoid and basal skin cells we obtained the green light dose dependency of the bilirubin phototoxicity to these cell types. Cells (3-5 x 10(6)/mL) were incubated with bilirubin complexed to human serum albumin (final concentrations 340 microM bilirubin, 150 microM albumin). Under these conditions all cells showed maximum binding of bilirubin. Irradiation with broadband green light (lambda max = 512 nm) over 24 h led to a light dose-dependent population of cells, which contained no bilirubin on the cell membrane as determined by Nomarski interference microscopy. The light-induced mechanism of the disappearance of bilirubin caused lethal membrane damage to the cells (trypan blue exclusion test). The cell kill rate increased with the irradiation dose and with the fraction of cells with no bilirubin. When 90% of lymphoid cells were bilirubin free, 46% of them were dead (using 480 J cm-1 green light). Similar results were obtained with basal skin cells. In addition, bilirubin-induced damage of cell membrane and nuclear membrane was also shown by transmission electron microscopy. Bilirubin (340 microM) in the dark led to 5% of the cells being killed. Basal skin cells bind 2.5 times more bilirubin molecules than lymphoid cells and showed a different bilirubin disappearance. Irradiation of bilirubin in carbon tetrachloride with 514.5 nm laser light showed generation of singlet oxygen via its luminescence at 1270 nm. These results demonstrate that green light phototherapy of hyperbilirubinemia may cause both skin and immune system damage.

Bilirubin↗
PubMed1994

Dietary carotenoids protect human cells from damage.

A physical chemistry technique based on singlet oxygen luminescence at about 1270 nm and a biological cell membrane technique were used to study the quenching of singlet oxygen by four carotenoids bound to the surface of lymphoid cells. All the carotenoids studied showed a beneficial effect in cell protection, but there were subtle differences between them.

Administration, Oral↗
PubMed1993

Cellular bound beta-carotene quenches singlet oxygen in man.

It is often postulated that a major role of carotenoids in biology and medicine involves their ability to quench a toxic form of oxygen, known as singlet oxygen, although direct observations of such mechanisms do not exist. Using beta-carotene, bound to lymphocytes taken from human blood, we have used a direct, pulsed laser, physical chemical technique and, separately, a biological method to show a particularly efficient quenching reaction of singlet oxygen by carotene in a cellular environment.

Carotenoids↗
PubMed1991

The phosphate pool of isolated dog heart during global ischaemia: comparison of two cardioplegic solutions with 31P NMR spectroscopy.

31P NMR spectroscopy was used to study the time course of changes in the concentration of high-energy metabolites and intracellular pH in the dog myocardium during hypothermic ischaemia at 9 degrees C in Bretschneider (HTK-B) and St. Thomas' Hospital (StTH) cardioplegic solutions. It was found that ATP and phosphocreatine degrade slowlier in HTK-B than in StTH, with phosphocreatine depletion occurring within 7.9 +/- 1.4 h in HTK-B and within 6.2 +/- 1.4 h in StTH. The values are virtually identical with the time intervals at which ATP concentration falls below the critical level (60% of initial ATP concentration). In agreement with biochemical analysis, a higher concentration of phosphomonoesters was noted until the 180th minute of ischaemia in HTK-B, a finding suggesting more rapid glycogen degradation in HTK-B. Even though HTK-B contains a high concentration of histidine buffer, higher values of intracellular pH were found during ischaemia in StTH. The effect of extracellular concentration of sodium ions on intracellular pH is discussed.

Adenosine Triphosphate↗
PubMed1990

[Cytotoxic effect on human keratinocytes caused by anti-Ro-(SS-A) antibodies and UVA in vitro].

It is supposed that anti-Ro(SS-A) antibodies play an important role in the development of photosensitive skin disease in subacute cutaneous lupus erythematosus and neonatal lupus erythematosus. The aim of the experiments was to demonstrate that anti-Ro(SS-A) antibodies and UVA-light cause a cytotoxic effect on human keratinocytes in vitro. Keratinocytes are irradiated with UVA-light in presence of serum containing anti-Ro(SS-A) antibodies (62 E, ELISA). After application of 20 J/cm2 UVA-light only 48.5% of the irradiated cells are still vital (standard trypan blue exclusions test). Examination by scanning electron microscopy shows plain depressions on the surface of the keratinocytes, which were irradiated in presence of anti-Ro(SS-A) antibodies.

Antibodies, Antinuclear↗
PubMed1990

[The cytotoxic effect of anti-Ro- (SS-A) antibodies and UVA light on human endothelial cells in vitro].

There is in photosensitive lupus erythematosus a strong association of high titers of anti-Ro(SS-A) antibodies in the serum of the patient with the development of special skin reactions depending on UV-light. The aim of our experiments was to detect a cytotoxic effect of anti-Ro(SS-A) antibodies and UVA-light on human endothelial cells in vitro (standard trypan blue exclusion test, SEM). After UVA-doses of 1 to 100 J/cm2, which were tested, and influence of serum containing anti-Ro(SS-A) antibodies (62 E, ELISA) membrane destructions of endothelial cells depending on the UVA-dose can be seen, irrespective of the fact whether the antibodies are present throughout the irradiation or added afterwards. This cytotoxic reaction depends on complement. A UVA-dose of 100 J/cm2 causes lethal damage of 40% of the cells. These results were confirmed by scanning electron microscopy.

Antibodies, Antinuclear↗
PubMed1988

[Therapeutic use of ultraviolet irradiation in medicine--scientific principles and clinical results].

Sunshine is one of mankind's oldest remedies. Merely forgotten, UV light treatment came back recently due to (1) technological progress, providing particular UV wavelengths (2) basic research, discovering mode of action at molecular level, and (3) rising knowledge about skin as the primary target. Human skin is a rather difficult organ, possessing a considerable part of the immune system, the so-called skin associated lymphoid tissue. Different biological effects are caused by UV irradiation at different wavelengths. UV radiation alone as well as together with a photosensitizer also can cause systemic effects. Dealing with these, results of basic research and their application on modern treatment of some skin diseases, transplantation medicine, non-specific resistance system, and treatment of cardiovascular diseases are discussed.

Animals↗
PubMed1986

PUVA therapy damages psoriatic and normal lymphoid cells within milliseconds.

Results of previous investigations have indicated that photochemotherapy (PUVA) attacks membranes of target cells. Using the combination of a stopped-flow technique and laser irradiation we were able to prove that the fast PUVA effect is explainable solely by the membrane damage. Lymphoid cells of healthy persons or psoriatics were taken, within 1 ms mixed with 8-methoxy-psoralen (8-MOP) at concentrations of 1.0, 0.1, and 0.5 microgram/ml, and then irradiated by a 337-nm laser pulse (0.5 mJ/cm2) lasting some picoseconds. Approximately 1 ms after administration of 8-MOP to the cell surface at least 10% of the cells were damaged, as could be judged using the standard trypan blue exclusion test. This happened at 8-MOP concentrations of 1.0 or 0.1 microgram/ml plus laser irradiation, but a concentration of 0.05 microgram/ml 8-MOP plus laser exposure did not cause any effect within 8 ms after mixing. There was no difference between using lymphoid cells from healthy persons or from psoriatics. The fact that only a very short time is necessary before cell damage occurs means that, as far as the fast PUVA effect is concerned, a photochemical reaction involving nuclear DNA can be discounted.

Cell Membrane↗