The role of DNA fragmentation in apoptosis

Bortner, Carl D.; Oldenburg, Nicklas B.E.; Cidlowski, John A.

doi:10.1016/s0962-8924(00)88932-1

Cited by 539 publications

(329 citation statements)

References 47 publications

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“…PrI staining, a widely used marker of necrotic death, cannot discriminate between primary necrosis and secondary necrosis in neurones that have undergone, perhaps simultaneously, an apoptotic death programme. It has been suggested that manipulations capable of blocking cell death (by using agents such as cycloheximide, actinomycin D, or ATA) are the most powerful methods of identifying apoptosis (Choi, 1996) and also that several criteria must be considered in the delineation of the death process (Bortner et al, 1995). For these reasons, a pragmatic view has been taken and the death described in this article has been called necrotic-or apoptotic-like, based on the morphological and biochemical resemblances to these respective pathways.…”

Section: Figurementioning

confidence: 99%

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

Staton

Bristow

1997

Journal of Neurochemistry

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Abstract:The neurotoxic properties of the dietary excitotoxins /3-N-methylamino-L-alanine and~3-N-oxalylamino-L-alanine have been studied in rat cerebellar granule cells and compared with those of glutamate. Glutamate caused dose-dependent death of cerebellar granule cells after a 30-min exposure when viability was assessed 24 h later. ß-N-Methylamino-L-alanine and /3-N-oxalylamino-L-alanine, however, were toxic only after 24 or 48 h of exposure. The neurotoxic effects of ß-N-methylaminO-L-alanine were blocked by D(-)-2-amino-5-phosphonopentanoic acid, and those of ß-N-oxalylamino-Lalanine were blocked by kynurenic acid, which demonstrated that these excitotoxins caused cerebellar granule cell death through the activation of glutamate receptors.

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Section: Figurementioning

confidence: 99%

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

Staton

Bristow

1997

Journal of Neurochemistry

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“…The initial dogma was that Zn directly inhibited: (1 ) Ca 2ϩ /Mg 2ϩ -dependent endonucleases that were responsible for DNA fragmentation (27); (2 ) the activity of caspase-3, a critical protease in apoptosis (28); or (3 ) the processing of caspase-3 (12,29). In Fas-induced apoptosis, Zn does not inhibit cytochrome c release and thus acts somewhere between cytochrome c release and caspase-3 activation, perhaps via cytochrome c interactions with capase-9, Apaf-1, or Bcl-X L (30).…”

Section: Zinc and Cell Deathmentioning

confidence: 99%

Nitric Oxide and Zinc Homeostasis in Acute Lung Injury

Croix

Leelavaninchkul²,

Watkins³

et al. 2005

Proceedings of the American Thoracic Society

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Among putative small molecules that affect sensitivity to acute lung injury, zinc and nitric oxide are potentially unique by virtue of their interdependence and dual capacities to be cytoprotective or injurious. Nitric oxide and zinc appear to be linked via an intracellular signaling pathway involving S-nitrosation of metallothoineinitself a small protein known to be an important inducible gene product that may modify lung injury. In the present article, we summarize recent efforts using genetic and fluorescence optical imaging techniques to: (1 ) demonstrate that S-nitrosation of metallothionein affects intracellular zinc homeostasis in intact pulmonary endothelial cells; and (2 ) reveal a protective role for this pathway in hyperoxic and LPS-induced injury.

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“…173,174 Morphologically, it is characterised by cellular features such as membrane blebbing, cell shrinkage and chromatin condensation. 175 Intracellular events include various types of DNA fragmentation, 176 cytoskeletal alterations and protease activation (reviewed in reference 177). There is increasing evidence that apoptosis is a cellular default setting, which must be actively suppressed (for example by growth factors, anti-apoptotic proteins) for the cell to survive.…”

Section: Apoptosis In Prostate Cancermentioning

confidence: 99%

Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

Costa-Pereira

Cotter

1999

Prostate Cancer Prostatic Dis

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Despite the high incidence and mortality rate of prostate cancer, the molecular mechanisms underlying the progression of the disease remain to be fully elucidated. This paper reviews the current state of knowledge on prostatic carcinogenesis, focusing not only on the molecular genetics of prostate cancer, but also on the role of oncogenes, tumour suppressor genes, and growth factors. The remarkable ability of prostate cancer cells to survive androgen withdrawal and apoptosis are discussed, with particular emphasis on how apoptosis may be manipulated from a therapeutic viewpoint.

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The role of DNA fragmentation in apoptosis

Cited by 539 publications

References 47 publications

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

The Dietary Excitotoxins β‐N‐Methylamino‐l‐Alanine and β‐N‐Oxalylamino‐l‐Alanine Induce Necrotic‐ and Apoptotic‐Like Death of Rat Cerebellar Granule Cells

Nitric Oxide and Zinc Homeostasis in Acute Lung Injury

Molecular and cellular biology of prostate cancer—the role of apoptosis as a target for therapy

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