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Biomedical subjects

T Ruzicka

Publications and source records attributed to T Ruzicka.

At least 361 records · Page 20Linked to original sources
PubMed1985

[Leukotrienes and monohydroxy fatty acids: controversial role in the pathogenesis of psoriasis].

The pros and cons concerning the involvement of arachidonic acid metabolism in the pathogenesis of psoriasis are presented. The isolation of arachidonic acid metabolites from psoriatic lesions, their extraordinary biological activity, and the therapeutic efficiency in psoriasis of inhibitors of arachidonic acid metabolism all argue in favor of leukotrienes and monohydroxy fatty acids playing an important role in the development of psoriasis plaques. On the other hand, the lack of specificity of the biochemical findings, the failure to reproduce psoriatic lesions by arachidonic acid metabolites, and the therapeutic activity of drugs that have no effect on arachidonic acid metabolism show that the role of arachidonic acid metabolism in the pathogenesis of psoriasis is still controversial. The availability of selective inhibitors of arachidonic acid-metabolizing enzymes for clinical testing is a prerequisite before pathophysiological conclusions can be made, as the present status of knowledge makes any conclusions premature.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1985

A probable case of rotavirus exanthem.

A generalized maculopapular exanthem and signs of hepatitis developed in a 28-year-old man one week after his two sons had suffered from rotavirus gastroenteritis. The patient's serum contained rotavirus antibody at titers of 1:256 and 1:512. Other known causes of exanthemata were excluded by clinical and laboratory investigations. The epidemiologic evidence and the results of serological tests suggested that the rotavirus caused the patient's exanthem.

Adult↗
PubMed1984

[Metabolism of arachidonic acid of the skin and its significance in the pathophysiology of inflammatory dermatosis].

Arachidonic acid can be converted via the cyclo-oxygenase and lipoxygenase pathways to biologically extremely potent products. The arachidonic acid metabolites - prostaglandins, prostacyclin, thromboxane, leukotrienes and hydroxy-fatty acids - are assumed to play a major role in the pathophysiology of inflammation. The skin shows an active arachidonic acid metabolism which is believed to be involved in the pathogenesis of psoriasis and different forms of dermatitis. Research into the biochemical basis of inflammation should lead to the introduction of new, pathogenetically oriented pharmacological principles in the treatment of these dermatoses.

Arachidonic Acids↗
PubMed1984

[Allergic vasculitis caused by vitamin B6].

A patient developed extensive bulloushaemorrhagic lesions on the lower legs after taking analgesic preparations. Allergologic tests yielded an Arthus-type reaction with vitamin B6. The histological and immunofluorescence examination of a lesional and test site biopsy showed the picture of a superficial and deep vasculitis with deposits of C3 at the basement membrane of dermal venules.

Aged↗
PubMed1983

Epidermal arachidonate lipoxygenase.

Guinea pig skin was found to display a high lipoxygenase activity, evidenced by the formation of a hydroxyeicosatetraenoic acid (HETE) from exogenous [14C]arachidonic acid. The lipoxygenase activity was localized to the epidermal layer of the skin, was completely inhibited by eicosatetraynoic acid (ETYA) and slightly enhanced by indomethacin. Susceptibility to inactivation by sulfhydryl-directed reagents indicated that an essential sulfhydryl is present in a hydrophobic region of the molecule. The enzyme exhibited a broad pH activity optimum and a Km of 2.48 . 10(-5) M. The cytosolic enzyme has been partly purified by ammonium sulfate precipitation and two steps of of column chromatography and exhibited an apparent high molecular weight. The lipoxygenase and hydroperoxidase activities were resolvable from one another. The physiological and pathophysiological roles of the enzyme remain to be elucidated.

Animals↗
PubMed1983

Cutaneous histamine levels and histamine releasability from the skin in atopic dermatitis and hyper-IgE-syndrome.

We determined the histamine content in the skin of 22 adults with atopic dermatitis, one patient with hyper-IgE-syndrome, and 20 controls by the enzymatic double isotope assay. In addition, we performed a pilot study of histamine degradation in the skin. We tested, furthermore, the releasability of histamine from skin sections of patients with atopic dermatitis and healthy controls upon challenge with acetylcholine, anti-IgE, and compound 48/80. Histamine was also determined in 13 plasma specimens and was always less than 1 ng/ml. The mean +/- SEM histamine concentration in the skin was 196 +/- 30 ng/mg protein in controls and 262 +/- 68 ng/mg protein in atopic dermatitis (no statistically significant difference). One control and three patients with atopic dermatitis exhibited a slight, the hyper-IgE patient a marked, elevation of the skin histamine content. No gross differences in the degradation rate of histamine were observed between patients and controls. Acetylcholine and 48/80 induced the same histamine release in both groups; with anti-IgE, almost the double amount of histamine was released from the skin of atopic dermatitis patients as compared to controls. These findings suggest an enhanced releasability of histamine upon immunologic challenge in atopic dermatitis.

Adolescent↗
PubMed1983

Inhibition of rat mast cell arachidonic acid cyclooxygenase by dapsone.

Dapsone (diaminodiphenylsulfone) has been used therapeutically for a variety of disorders in which mast cell participation has been demonstrated, including bullous pemphigoid and some form of necrotizing vasculitis. The mechanism of action of dapsone in these disorders is unknown but potentially relates to inhibition of mast cell activation and prevention of generation and/or release of mast cell mediators. Evidence for this possibility has been obtained in rat mast cells in which dapsone in a concentration-dependent manner prevented generation of prostaglandin D2 PGD2 from exogenous or endogenous arachidonic acid with 50% inhibition achieved at 1 and 0.2 to 0.4 mM, respectively. Dapsone inhibited cyclooxygenase conversion of arachidonic acid to PGD2 but not the GSH-dependent conversion of 14C-PGH2 to PGD2 by PGH-D isomerase in broken cell preparations. Dapsone prevented the immunologic generation of PGD2 from antigen-challenged rat mast cells but did not affect the release of histamine. Thus dapsone may exert some of its therapeutic effects by prevention of mast cell PGD2 generation.

Animals↗
PubMed1983

Changes in arachidonic acid metabolism in UV-irradiated hairless mouse skin.

This study was conducted to investigate the metabolism of arachidonic acid in the skin of hairless mice exposed to UVA, PUVA, UVB, and UVC irradiation. The main products of arachidonic acid in the epidermis were hydroxyeicosatetraenoic acid (HETE), PGE2, and PGD2. Dermis displayed a lower lipoxygenase activity (expressed as HETE production) than the epidermis and showed no detectable cyclooxygenase activity, i.e., no prostaglandin production. The main changes observed in UV-induced inflammatory reactions were as follows. 1. A 5-fold increase in dermal HETE production in PUVA-treated animals and a 29% reduction in epidermal HETE formation after UVC treatment. 2. A marked decrease of PGD2 and a marked increase of PGE2 formation due to alterations of PGH2 metabolism in the UVB-treated group; however, cyclooxygenase activity was unchanged. These changes in arachidonic acid metabolism in the skin may be of pathophysiologic importance in UV-induced inflammatory reaction.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Arachidonic acid metabolism in guinea pig skin.

Studies were conducted to examine the metabolism of radioactively labelled arachidonic acid via the lipoxygenase and cyclooxygenase pathways and the metabolic conversions of radioactively labelled prostaglandin H2 in the epidermal and dermal layers of the guinea-pig skin. Arachidonic acid was metabolized preferentially via lipoxygenase to hydroxyeicosatetraenoic acid (HETE). The major product of the cyclooxygenase pathway was prostaglandin D2; prostaglandin E2 was formed in lesser amounts. Epidermis exhibited much higher activities of these enzymes on a milligram protein basis than the dermis. In contrast, both skin layers showed the same very high activity of GSH-dependent prostaglandin H2/prostaglandin D2 isomerase; Prostaglandin D2 was virtually the only product formed by skin homogenates from prostaglandin H2. Guinea-pig skin is a highly active site of arachidonic acid metabolism. These findings will provide the basis for pathobiochemical studies in inflammatory and hyperproliferative dermatoses.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Arachidonic acid metabolism in guinea pig skin: effects of chloroquine.

We investigated the effect of chloroquine (CQ) on the metabolism of exogenous [14C]arachidonic acid by guinea pig skin homogenates. The major cyclooxygenase product formed by the homogenates was PGD2; smaller quantities of PGE2 were formed. CQ suppressed the production of PGD2 and PGE2 in a dose-dependent fashion with an IC50 of 230 microM. This suppression was due to a cyclooxygenase inhibition, since the formation of the prostaglandins from exogenous endoperoxide PGH2 was unaffected. The skin homogenates also exhibited an active lipoxygenase pathway leading to HETE formation. The effect of CQ on the lipoxygenase activity was far less marked than its effect on the cyclooxygenase. CQ is an inhibitor of the cutaneous cyclooxygenase, and this effect may contribute to its anti-inflammatory action in various dermatological disorders.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1982

Arachidonic acid metabolism in skin: experimental contact dermatitis in guinea pigs.

The cutaneous metabolism of exogenous arachidonic acid and endoperoxide (PGH2) to prostaglandins and hydroxy-fatty acids was investigated in experimental contact dermatitis in guinea pigs and compared to normal skin, unsensitized animals treated with the allergen dinitrochlorobenzene, and Trafuril-induced irritant dermatitis. The main alterations of cutaneous arachidonate metabolism in contact dermatitis comprise: (1) an inhibition of PGD2 synthesis; (2) a switch from predominant PGD2 production to a predominance of PGE2 and (3) a marked inhibition of the lipoxygenase activity.

Animals↗
PubMed1981

Effects of dapsone on passive Arthus reaction and chemotaxis and phagocytosis of polymorphonuclear leukocytes.

The effects of dapsone (diaminodiphenyl sulfone) on the polymorphonuclear leukocyte (PMNL) function and on the elicitation of the passive Arthus reaction were investigated in rabbits and guinea-pigs. NBT-reduction was markedly enhanced in PMNL of animal receiving 5 mg dapsone/kg for 3 days, whereas chemotaxis and phagocytosis were not influenced. Passive Arthus reaction was clearly suppressed by the same treatment regimen. 2 mg/kg of the drug had no effect on the parameters examined.

Animals↗
PubMed1981

Dapsone in the treatment of lupus erythematosus.

Dapsone yielded excellent therapeutic results in certain forms of lupus erythematosus (LE), whereas discoid lesions and the maculo-papular rash of the systemic and disseminated chronic forms of discoid LE remained uninfluenced by the drug. On the basis of these observations, we suggest the following indications for dapsone treatment in LE: (1) Vasculitic urticaria. (2) Oral ulceration. (3) Non-scarring form of chronic LE. (4) Chloroquine intolerance.

Adult↗