3-Hydroxykynurenine as a Potential Ligand for Hsp70 Proteins and Its Effects on Drosophila Memory After Heat Shock

Abstract Kynurenine products of tryptophan metabolism are modifiers of the nervous activity and oxidative processes in mammals and invertebrates. 3-hydroxykynurenine (3HOK) in moderate concentrations is a lipid peroxidation inhibitor. However, its accumulation and oxidative auto dimerization lead to oxidative stress development manifested in age-related neurodegenerative diseases (NDDs) and neurologic disorders provoked by acute stress. Different forms of stress, the mostly studied being heat shock response, rely on functioning of heat shock proteins of Hsp70 superfamily. Since kynurenines are called “kids of stress”, we performed computational estimation of affinity of 3HOK and other kynurenines binding to predicted ATP site of Drosophila Hsp70 cognate 71 protein (Dhsp71) using Autodock Vina. The binding energy of 3HOK dimer is -9.4 kcal/mol, its orientation within the active site is close to that of ATP. This might be a new mechanism of producing a competitive inhibitor of Hsp70 chaperones that decreases organism ability to adapt to heat shock. We also showed that the Drosophila melanogaster cardinal (cd1) mutant with 3HOK excess, serving as a model for Huntington's disease (HD), manifests severe defects of short-term memory after heat shock applied either in adults, or at the prepupal stage.

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Fish kidney cell line in response to heat shock

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100123921 ◽

1992 ◽

Vol 50 (1) ◽

pp. 704-705

Author(s):

Li-Chu Tung ◽

Yung-Reui Chen ◽

Shiu-Nan Chen ◽

Guang-Hsiung Kuo

Keyword(s):

Heat Shock ◽

Cell Line ◽

Fetal Calf Serum ◽

Calf Serum ◽

Uranyl Acetate ◽

Ultrastructural Changes ◽

Heat Shock Treatment ◽

Acanthopagrus Schlegeli ◽

Cacodylate Buffer ◽

Fish Kidney

In the present study, the ultrastructural changes of BPK cells, a fibroblast-like cell line, derived from the kidney of juvenile black porgy Acanthopagrus schlegeli, under heat shock treatment are described.The BPK cells were maintained in L-15 medium supplemented with 10% fetal calf serum and 0.15 M NaCl at 28|C2. The heating was carried out in precalibrated water baths. Monolayers of cells, grown on coverslips in parafilm-sealed petri dishes were submerged under water for 30 min at 40|C treatments. Cells were fixed in 2.5% glutaraldehyde in 0.1 M cacodylate buffer supplemented with 6.6% sucrose, postfixed in 1% OsO4 and flat embedded in Spurr’s resin. Silver section were cut parallel to the substratum, stained with uranyl acetate and Reynold’s lead citrate, and examined in a Hitachi H-600 electron microscope at 75 KV.

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Absence of temporal ordering of apoptotic features in heat-shock treated leukemia and lymphoma cell lines

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100166257 ◽

1996 ◽

Vol 54 ◽

pp. 758-759

Author(s):

D. W. Fairbain ◽

M.D. Standing ◽

K.L. O'Neill

Keyword(s):

Heat Shock ◽

Cell Lines ◽

Chromatin Condensation ◽

Membrane Integrity ◽

Resistant Cell ◽

Membrane Blebbing ◽

Late Loss ◽

Induced Apoptosis ◽

Dying Cells ◽

In Cells

Apoptosis is a genetically defined response to physiological stimuli that results in cellular suicide. Features common to apoptotic cells include chromatin condensation, oligonucleosomal DNA fragmentation, membrane blebbing, nuclear destruction, and late loss of ability to exclude vital dyes. These characteristics contrast markedly from pathological necrosis, in which membrane integrity loss is demonstrated early, and other features of apoptosis, which allow a non-inflammatory removal of dead and dying cells, are absent. Using heat shock-induced apoptosis as a model for examining stress response in cells, we undertook to categorize a variety of human leukemias and lymphomas with regard to their response to heat shock. We were also interested in determining whether a common temporal order was followed in cells dying by apoptosis. In addition, based on our previous results, we investigated whether increasing heat load resulted in increased apoptosis, with particular interest in relatively resistant cell lines, or whether the mode of death changed from apoptosis to necrosis.

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