2-butenal and Necrosis

Crotonaldehyde is a common environmental contaminant. Autophagy, apoptosis, and necrosis, were all respectively reported to be induced by crotonaldehyde. However, the relationships between programmed cell deaths, especially between autophagy and apoptosis, have not been elucidated. In the present study, alterations of autophagy, apoptosis and necrosis were investigated in human bronchial epithelial cells (BEAS-2B) exposed to crotonaldehyde, and effects of autophagy on apoptosis and necrosis were detected. We found that a high concentration (160 μmol/L, μM) of crotonaldehyde did not induce apoptosis, while a low concentration (80 μM) of crotonaldehyde induced autophagy, apoptosis and necrosis. In 80 μM crotonaldehyde-exposed BEAS-2B cells, autophagy and apoptosis exhibited a trend of increasing prior to decreasing with the increase of time, while the time point inducing the highest level of autophagy was 2 h, and that of apoptosis was 4 h. With the pretreatment of bafilomycin A

Topics: Aldehydes; Apoptosis; Autophagy; Bronchi; Cell Line; Enzyme Inhibitors; Epithelial Cells; Humans; Macrolides; Necrosis

The irritating aldehyde acrolein was injected intraperitoneally into mice. A single injection at 4 mg/kg gave rise to a 5-fold increase in plasma total lactate dehydrogenase (LDH) activity, with the peak after approximately 10 h. The pattern of LDH isoenzymes was not altered. Repeated injections (daily or weekly) caused a progressively less pronounced effect on the LDH activity. Experiments with formaldehyde and crotonaldehyde gave essentially the same results. The LD50 for acrolein i.p. in mice was increased from a level of 7 mg/kg to a level of 12 mg/kg by pretreatment with sublethal doses of 4 mg/kg/day for 5 days. Thus, the response to repeated acrolein injections, in terms of LDH and LD50, indicates an acquired tolerance against the irritant. Likewise, pretreatment with formaldehyde or crotonaldehyde could induce tolerance, in terms of LDH activity, towards a subsequent injection of acrolein. Histopathological examination revealed that spleen, adrenals and thymus were affected. The thymus markedly decreased in size after repeated injections of acrolein, crotonaldehyde or formaldehyde. Adrenalectomized mice given acrolein showed no thymus atrophy. A single injection of aldehyde caused an increased level of the adrenal hormone corticosterone in blood plasma. Adrenalectomized mice still showed a certain tolerance, in terms of LDH activity, after repeated injections of acrolein, but the increase in plasma LDH activity was smaller than for normal animals. Treatment with acrolein for six days did not change the level of reduced glutathione or the glutathione S-transferase activity in liver cytosol, but the rate of glutathione synthesis was increased. It is concluded that adrenalectomy does not completely prevent the development of tolerance in mice. It is possible that an increased metabolism can partially explain the acquired tolerance.

Topics: Acrolein; Adrenal Glands; Aldehydes; Animals; Atrophy; Corticosterone; Dose-Response Relationship, Drug; Erythrocytes; Formaldehyde; Inactivation, Metabolic; L-Lactate Dehydrogenase; Liver; Mice; Necrosis; Spleen; Thymus Gland