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PubMed1990

Temperature and anation studies of the type 2 site in Rhus vernicifera laccase.

Temperature-dependent structural changes involving the type 2 site in laccase are probed by EPR studies of a derivative of laccase in which the type 1 Cu has been replaced by Hg(II) [Morie-Bebel, M. M., Morris, M. C., Menzie, J. L., & McMillin, D. R. (1984) J. Am. Chem. Soc. 106, 3677-3678]. At the temperature extremes (123 and 299 K), single well-defined species are present, but at intermediate temperatures (between 213 and 253 K), the presence of multiple structures is indicated. For the first time, the room temperature EPR spectrum of the type 2 copper has been resolved. Azide binding and fluoride binding have also been studied as a function of temperature. The results suggest that each anion preferentially interacts with the type 3 site in fluid solution and that these adducts can be trapped by rapidly cooling the sample to 123 K. Annealing the adducts at 253 K permits rearrangement and binding at an equatorial position of the type 2 Cu. This pathway to anation at the type 2 site contrasts sharply with previous studies which required a large excess of anions, and it reveals important insight into the flexibility of the type 2/type 3 cluster in laccase.

Electron Spin Resonance Spectroscopy↗
PubMed1991

Modulation of leucocyte adhesion molecules, a T-cell chemotaxin (IL-8) and a regulatory cytokine (TNF-alpha) in allergic contact dermatitis (rhus dermatitis).

To understand the molecular events which are important in leucocyte trafficking in cutaneous inflammation, poison ivy/oak extract was applied topically to the skin, and the simultaneous assessment of a variety of clinical and immunopathological parameters performed. The clinical response of subjects was divided into three main groups: I, 2-24h after application, before the onset of erythema; II, 48 h-1 week after application during maximal clinical changes; III, 2-3 weeks after application when the inflammation had subsided. Six different biopsies per subject were evaluated over the study period and the density of dermal cellular infiltrate, and the distribution of intercellular adhesion molecule-1, (ICAM-1), endothelial leucocyte adhesion molecule-1, (ELAM-1), vascular cell adhesion molecule-1, (VCAM-1), interleukin 8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha), determined. Eight hours after exposure, before lymphocytes and monocytes had entered the dermal interstitium or epidermis, the keratinocytes expressed TNF-alpha and ICAM-1, whilst the endothelial cells expressed ELAM-1, VCAM-1 and ICAM-1. Group II biopsies revealed increasing keratinocyte expression of TNF-alpha and ICAM-1 with the appearance of IL-8, which correlated with the onset of epidermal T-cell trafficking. The endothelium was strongly positive for ELAM-1 and VCAM-1, but there was no influx of neutrophils. Group III biopsies showed a decrease in the expression of ICAM-1, VCAM-1 and ELAM-1 by both keratinocytes and endothelium with a reduction in epidermal/dermal inflammation, although the endothelial cell staining of VCAM-1 and ELAM-1 did not completely disappear. These results suggest that on exposure to poison ivy/oak, keratinocytes rapidly produce TNF-alpha which leads to an early autoinduction of ICAM-1, and later IL-8. There is also a paracrinemediated induction and augmentation of underlying endothelial cell ELAM-1, VCAM-1 and ICAM-1.

Adult↗