Programmed cell death during metamorphosis in the blow-flyCalliphora vomitoria

Bowen, I. D.; Mullarkey, K.; Morgan, Sara

doi:10.1002/(sici)1097-0029(19960615)34:3<202::aid-jemt3>3.0.co;2-r

Cited by 61 publications

(32 citation statements)

References 56 publications

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“…Cellular death can occur either by accident, referred to as necrosis, or by design variously described as physiological cell death, programmed cell death or apoptosis (Bowen et al 1996). Apoptosis presents a range of morphological symptoms including cell shrinkage, chromatin margination followed by DNA fragmentation and a florid break-up of the cell into spherical apoptotic bodies (Wyllie 1981).…”

Section: Epithelioma Papulosum Cyprini Cell Death Necrosis Immunohmentioning

confidence: 99%

“…The subsequent morphological changes encompass oedema following calcium overload, dilatation of the endoplasmic reticulum, polysome disaggregation, and mitochondrial swelling. The chromatin condenses, and clumps are formed at the nuclear periphery (Bowen et al 1996). Necrosis refers to the post mortem changes that occur following the death of the cell (Trump and Berezesky 1998).…”

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Infectious Haematopoietic Necrosis Virus-Induced Cell Death in Fish Cell Culture

Gregorc¹,

Bowen²,

JENâIâ³

et al. 2005

Acta Vet. Brno

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Cell death development was investigated in the epithelioma papulosum cyprini (EPC) cell line after infection with infectious haematopoietic necrosis virus (IHNV). Cytopathic effect (CPE) was evaluated, immunohistochemistry for virus localisation and the development of cell death were studied. Modes of cell death were characterised by staining with TdT-mediated dUTP nick end labelling (TUNEL), and with Annexin V and propidium iodide.CPE was evaluated as 25%, 50%, 75% and 100% at the virus culture infective concentration doses (TCID50/0.1 ml) of 1. 25, 6.25, 31.25 and 156.25, respectively, and no CPE was found at the concentration lower than 0.25 TCID50/0.1ml. At the PBS:virus concentration 0.25 TCID50/0.1 ml only a few cells were found anti IHNV antibody positive, and no CPE was observed. In the range of virus concentrations from 6.25 to 156.25 TCID50/0.1 ml all cells were positive. The level of positive cells using the TUNEL technique increased 30% and 55% after the increasing the CPE up to 50% and 75%, respectively. At the higher levels of CPE, all the remaining cells were positive.Infected cells exhibited features of early stage of apoptosis as demonstrated reactivity with annexin V. Apoptotic cells expose external phosphatidylserine residues while preserving membrane integrity. Red fluorescence with propidium iodide is associated with increased levels of necrosis and appeared in cells simultaneously with FITC marker and also alone in vacuolated and enlarged necrotic cells. Apoptosis appears before the pathological changes of necrosis and it is correlated to the spread of infection. The relevance of the current view that IHNV infection includes at least two modes of cell death: apoptosis and necrosis, is discussed. Epithelioma papulosum cyprini, cell death, necrosis, immunohistochemistry, annexin V, TUNELCellular death can occur either by accident, referred to as necrosis, or by design variously described as physiological cell death, programmed cell death or apoptosis (Bowen et al. 1996). Apoptosis presents a range of morphological symptoms including cell shrinkage, chromatin margination followed by DNA fragmentation and a florid break-up of the cell into spherical apoptotic bodies (Wyllie 1981). It has been shown that apoptosis can be induced by genetic means (Ellis et al. 1991), but can also be induced by non-genetic means (Arends and Wyllie 1991). Necrotic cell death appears to be induced under extreme conditions such as ischaemia, hypoxia, toxin, hyperthermia. The subsequent morphological changes encompass oedema following calcium overload, dilatation of the endoplasmic reticulum, polysome disaggregation, and mitochondrial swelling. The chromatin condenses, and clumps are formed at the nuclear periphery (Bowen et al. 1996). Necrosis refers to the post mortem changes that occur following the death of the cell (Trump and Berezesky 1998).A range of approaches are available to demonstrate the apoptosis of cells in living tissue or cell suspensions. Immunocytochemical methods assaying DNA fragmentation (Trauth ...

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Section: Epithelioma Papulosum Cyprini Cell Death Necrosis Immunohmentioning

confidence: 99%

mentioning

confidence: 99%

Infectious Haematopoietic Necrosis Virus-Induced Cell Death in Fish Cell Culture

Gregorc¹,

Bowen²,

JENâIâ³

et al. 2005

Acta Vet. Brno

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“…This type of cell death can be induced by genetic means (White, 1996). Apoptosis is a particular form of programmed cell death such as in normal cell turnover, while necrotic cell death appears to be induced after a lethal accident or disease and under extreme conditions such as ischaemia, hypoxia, exposure to toxins and hyperthermia (Bowen et al, 1996). Apoptosis can be detected in situ using the terminal deoxynucleotidyl transferase mediated dUDP nick end labelling (TUNEL) method (Orita et al, 1999;Pulkkanen et al, 2000;Ortiz, 2003).…”

Section: Introductionmentioning

confidence: 99%

Toxicological and immunohistochemical testing of honeybees after oxalic acid and rotenone treatments

Gregorc

Škerl

2007

Apidologie

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-Bees removed capped brood and young larvae from combs at a greater rate after a rotenone treatment than after an oxalic acid (OA)/sucrose treatment. Rotenone (1%) caused 75.2% of capped brood to be removed, OA (3%) 18.7% and a control treatment, 13.3%. Caged worker bees treated with a 1% rotenone powder, a 3% OA or with a control solution had mortality rates of 10.9%, 5.1% and 1.9% respectively. Rotenone (1%) significantly affected the mortality of brood and adult bees whereas OA (3%), did not. Solutions of 3% OA/32% sucrose, 3.4% OA/47.6% sucrose, 3.7% OA/27.1% sucrose (w/w) and a 32% sugar solution applied to adult bees resulted in death rates of 11%, 14%, 11.2% and 6.5% respectively. Individually treated bees consumed more of a 3% OA solution than solutions with higher OA concentrations. A TUNEL assay detected necrotic cell death in 69% of bee midgut cells 24 h after an OA treatment. Normal cell turnover is approximately 8%.Treatment / Apis mellifera / acaricide / TUNEL / cell death / mortality

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“…It could be argued that if programmed cell deaths, until very recently clumped together under the term "apoptotic", do not constitute a homogeneous category, but may be classified on the basis of highly diagnostic ultrastructural images as a) apoptosis, b) atrophy, and c) differentiation (Bowen et al 1996), then accidental cell deaths may also fall into a variety of categories. Unfortunately, the prevailing view is still that accidental cell deaths collectively conform to a single form of `necrosis'.…”

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confidence: 99%

“…Unfortunately, the prevailing view is still that accidental cell deaths collectively conform to a single form of `necrosis'. The latter is thought to pass along the following regular chain of events: calcium overload with subsequent cell oedema, dilation of endoplasmic reticulum, polysome disintegration, and mitochondrial swelling (Bowen et al 1996).…”

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confidence: 99%

Cylotogical Postmortem Changes in Highly Specialized Cells Subjected to Different Causes of Necrosis.

Meyer‐Rochow

Järvilehto

1997

CYTOLOGIA

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Programmed cell death during metamorphosis in the blow-flyCalliphora vomitoria

Cited by 61 publications

References 56 publications

Infectious Haematopoietic Necrosis Virus-Induced Cell Death in Fish Cell Culture

Infectious Haematopoietic Necrosis Virus-Induced Cell Death in Fish Cell Culture

Toxicological and immunohistochemical testing of honeybees after oxalic acid and rotenone treatments

Cylotogical Postmortem Changes in Highly Specialized Cells Subjected to Different Causes of Necrosis.

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