Biomedical subjects

D J Allan

Publications and source records attributed to D J Allan.

26 records · Page 2Linked to original sources

PubMed1988

The behaviour of chickens, mice and rats during euthanasia with chloroform, carbon dioxide and ether.

Euthanasia of chickens, young and mature rats, and mice was assessed using chloroform, carbon dioxide and ether. Behavioural patterns were recorded to give some indication of the stress involved. Carbon dioxide induced collapse faster (11.2 +/- 0.4 s) than chloroform (18.9 +/- 0.4 s) or ether (greater than 60 s). With regard to the time taken to death, in carbon dioxide mice had the shortest time (48 +/- 10 s) and mature rats had the longest time (135 +/- 10 s). In chloroform, the only difference was the delayed onset of death (127 +/- 10 s) in the chicken. Behavioural patterns were similar for the chicken in carbon dioxide and chloroform, except for wing flapping, even when unconscious, in carbon dioxide. Chloroform is recommended as more aesthetically acceptable for euthanasia of chickens. Carbon dioxide is recommended for the euthanasia of both rats and mice, considering behavioural criteria. Ether is unsuitable as a euthanasia method as it is dangerous, slow acting and an irritant.

Animals↗

PubMed1988

Sertoli cell death by apoptosis in the immature rat testis following x-irradiation.

The importance of the morphological study of cell death has recently been emphasized by the recognition that the ultrastructural features of dying cells allow categorization of the death as either apoptosis or necrosis. This classification enables inferences to be drawn about the mechanism and biological significance of the death occurring in a particular set of circumstances. In this study, Sertoli cell death induced in the immature testis of three and four day old rats by 5 Gy (500 rads) x-irradiation was described by light and transmission electron microscopy with the objective of categorizing the death as apoptosis or necrosis. The testes were examined 1, 2, 3, 4, 8, and 24 h after irradiation. Following irradiation, there was a wave of apoptosis of the Sertoli cells starting in three to four hours and reaching a peak between four and eight hours. At 24 hours, only 61% of the expected number of Sertoli cells remained. These findings are in accord with recent ultrastructural reports that ionizing radiation induces cell death by apoptosis in rapidly proliferating cell populations. New insights into the pathogenesis of radiation-induced cell death might thus be expected to stem from future elucidation of the general molecular events involved in triggering apoptosis.

Animals↗

PubMed1988

X-ray-induced cell death by apoptosis in the immature rat cerebellum.

The cells of the external granular layer (EGL) of the developing cerebellum are known to be particularly sensitive to radiation. In the past, changes induced in this layer by irradiation have been referred to by non-specific terms such as "pyknotic cells" and the mode of cell death has been assumed to be necrosis. However, in published light micrographs of these dying cells, the appearance is suggestive of apoptosis, a distinctive mode of cell death which occurs spontaneously in normal adult and embryonic tissues and can also be triggered by certain pathological stimuli. This light and transmission electron microscopic study of control and irradiated (7 h post-irradiation) rat cerebellum from 18 day fetuses and 5 day-old neonates showed that the cell death was effected by apoptosis. The apoptosis was markedly enhanced by x-irradiation and quantification of the cell death in the EGL of 5 day-old rats exposed to 4, 8, 25, 100, and 400 cGy x-irradiation demonstrated that there was a positive dose response relationship. The extent of cell death by apoptosis which was 0.2% in control, ranged from 0.8% after 4 cGy to 62.3% after 400 cGy x-irradiation. The recognition that cell death by apoptosis can be a major component of x-irradiation damage has important implications for radiobiological studies.

Animals↗

PubMed1986

The morphologic categorization of cell death induced by mild hyperthermia and comparison with death induced by ionizing radiation and cytotoxic drugs.

This paper presents a summary of the morphological categorization of cell death, results of two in vivo studies on the cell death induced by mild hyperthermia in rat small intestine and mouse mastocytoma, and a comparison of the cell death induced by hyperthermia, radiation and cytotoxic drugs. Two distinct forms of cell death, apoptosis and necrosis, can be recognized on morphologic grounds. Apoptosis appears to be a process of active cellular self-destruction to which a biologically meaningful role can usually be attributed, whereas necrosis is a passive degenerative phenomenon that results from irreversible cellular injury. Light and transmission electron microscopic studies showed that lower body hyperthermia (43 degrees C for 30 min) induced only apoptosis of intestinal epithelial cells, and of lymphocytes, plasma cells, and eosinophils. In the mastocytoma, hyperthermia (43 degrees C for 15 min) produced widespread tumor necrosis and also enhanced apoptosis of tumor cells. Ionizing radiation and cytotoxic drugs are also known to induce apoptosis in a variety of tissues. It is attractive to speculate that DNA damage by each agent is the common event which triggers the same process of active cellular self-destruction that characteristically effects selective cell deletion in normal tissue homeostasis.

Animals↗

PubMed1985