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Journal ArticleDOI

Apoptosis induced in macrophages and T blasts by the mycotoxin sporidesmin and protection by Zn2+ salts.

TLDR
The inhibition of apoptosis induced by ETP compounds by Zn2+ appears to be due to direct inhibition of oxidative damage to plasmid DNA in vitro by inhibiting auto-oxidation of the reduced ETP compound because of the looseness of the interaction.
About
This article is published in International Journal of Immunopharmacology.The article was published on 1990-01-01. It has received 70 citations till now. The article focuses on the topics: Gliotoxin & Programmed cell death.

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Specific Proteolytic Cleavage of Poly(ADP-ribose) Polymerase: An Early Marker of Chemotherapy-induced Apoptosis

TL;DR: The results suggest that proteolytic cleavage of pADPRp, in addition to being an early marker of chemotherapy-induced apoptosis, might reflect more widespread proteolysis that is a critical biochemical event early during the process of physiological cell death.
Journal ArticleDOI

Zinc and immune function: the biological basis of altered resistance to infection.

TL;DR: Parts of zinc biology of the immune system are explored and a biological basis for the altered host resistance to infections observed during zinc deficiency and supplementation is attempted.
Journal ArticleDOI

Apoptosis: the biochemistry and molecular biology of programmed cell death.

TL;DR: This review first briefly covers some historical perspective on the discovery of apoptotic cell death, the characteristic morphology that accompanies this process, and the numerous cell types and mediators with which programmed cell death is associated.
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The role of zinc in caspase activation and apoptotic cell death

TL;DR: The purpose of this review is to integrate previously published knowledge on Zn and apoptosis with current attempts to elucidate the mechanisms of action of this biometal, and examine the cytoprotective functions of Zn which suppress major pathways leading to apoptosis, as well as the more direct influence of ZN on the apoptotic regulators, especially the caspase family of enzymes.
Journal Article

Activated murine macrophages induce apoptosis in tumor cells through nitric oxide-dependent or -independent mechanisms.

TL;DR: The role of apoptosis as a mechanism for nitric oxide (NO)-mediated macrophage tumor cytotoxicity and the anti-tumor necrosis factor alpha monoclonal antibody fully prevented apoptosis when macrophages and L929 were separated by a cell-impermeable membrane are investigated.
References
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Book

Molecular Cloning: A Laboratory Manual

TL;DR: Molecular Cloning has served as the foundation of technical expertise in labs worldwide for 30 years as mentioned in this paper and has been so popular, or so influential, that no other manual has been more widely used and influential.
Journal ArticleDOI

Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation

A. H. Wyllie
- 10 Apr 1980 - 
TL;DR: It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
Journal Article

Glucocorticoid activation of a calcium-dependent endonuclease in thymocyte nuclei leads to cell death.

TL;DR: It appears that glucocorticoids cause thymocyte death by activating an enzyme that rapidly and extensively degrades DNA, and it is suggested that it may be part of a system for transporting calcium into the nucleus.
Journal ArticleDOI

Chromatin sub-structure. The digestion of chromatin DNA at regularly spaced sites by a nuclear deoxyribonuclease.

TL;DR: Evidence is presented that indicates a regular sub-structure in nuclear nucleoprotein with regularly distributed sites that are specifically susceptible to the cellular Ca-Mg endonuclease.
Journal ArticleDOI

Immunosuppression in vitro by a metabolite of a human pathogenic fungus

TL;DR: Inhibition of cytotoxic T-cell induction by gliotoxin at low concentrations, acting on the stimulator cells, can be overridden by concanavalin A-activated cell supernatants and the possible role of gliot toxin in the etiology of A. fumigatus-related diseases is discussed.
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