Effect of Cycloheximide on the Cell Cycle of the Crypts of the Small Intestine of the Rat

“…Nonetheless a few studies show that inhibition of protein synthesis is lethal mainly to lymphocyte populations, and does not eliminate mitoses throughout the whole body (28,29). One explanation might be that different cells and tissues in the same organism show wide variations as to the kinetics of cell death.…”

mentioning

confidence: 99%

Cell death: Apoptosis versus necrosis (Review)

Kanduc¹,

Mittelman²,

Serpico³

et al. 2002

Int J Oncol

239

242

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. Cell death and the subsequent post-mortem changes, called necrosis, are integral parts of normal development and maturation cycle. Despite the importance of this process, the mechanisms underlying cell death are still poorly understood. In the recent literature, cell death is said to occur by two alternative, opposite modes: apoptosis, a programmed, managed form of cell death, and necrosis, an unordered and accidental form of cellular dying. The incorrect consequence is the overlapping of: a) the process whereby cells die, cell death; and b) the changes that the cells and tissues undergo after the cells die. Only the latter process can be referred to as necrosis and represents a 'no return' process in cell life. In this review, we discuss the excellent basic research developed in this field during last decades and problems that remain to be resolved in defining both experimentally and mechanicistically the events that lead to and characterize cell death. IntroductionCell death is part of normal development and maturation cycle, and is the component of many response patterns of living tissues to xenobiotic agents (i.e. micro organisms and chemicals) and to endogenous modulations, such as inflammation and disturbed blood supply (1,2). Cell death is an important variable in cancer development, cancer prevention and cancer therapy (3-5). In the treatment of cancer, the major approach is the removal, by surgery, of the neoplasm and/or the induction of cell death in neoplastic cells by radiation, toxic chemicals, antibodies and/or cells of the immune system (6-9). On the other hand, this pathobiological process remains poorly understood and the physiological and biochemical factors that lead to cell death are still not clear. One main factor is the existing confusion between 'apoptosis' process, as compared and contrasted with 'necrosis', leading to the overlapping of the ante mortem changes, i.e. the process of cell death, and the post-mortem changes, i.e. the necrosis process. The pathobiology of cell deathThe elegant scientific exploration of sub-cellular molecular anatomy of the last decades have reinforced the cell concept as 'the smallest integrating unit in biology: a pseudo-intelligent computer that receives, screens, changes, reacts to and adapts to a host of environmental signals, all of this activity apparently

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“…As in the case of cycloheximide treatment (Nakagawa and Nagai , 1971), gluconeogenesis may be blocked by inhibition of de nova synthesis of the key enzymes that is indispensable to the increase in enzymatic activities . As a noncytotoxic inhibitor of protein synthesis, cycloheximide induces complete disappearanec of mitotic figures in the crypt cells during 1.5-2.0 hr, by blocking G2 phase of the cell cycle (Verbin and Farber, 1967); while FX, by blocking all phases of the cell cycle (Ohtsubo, Yamada and Saito, 1968), inhibits the mitosis completely in 1 hr. X-ray irradiation is very similar to FX treatment in causing mitotic inhibition in the intestinal crypt cells, followed by cell degeneration and necrosis (Bloom and Fawcett, 1968).…”

Section: Glucose Tolerance Testmentioning

confidence: 99%

Hypoglycemia in Mice Administered With Fusarenon-X

Shimizu

Nakano

Matsui

et al. 1979

JJMSB

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SUMMARY: Histological observation combined with determination of the serum glucose level and histochemical detection of liver glycogen was undertaken to examine the acute toxicity of fusarenon-X (FX) in mice. Mice intraperitoneally injected with a sublethal dose of the toxin showed rapidly developed hypoglycemia followed by depletion of liver glycogen. Mitotic inhibition was observed in many visceral organs and most markedly in the intestinal crypt cells, where the mitotic figures completely disappeared prior to the increase in number of the degenerated and necrotic cells. No glycosuria was found. The disturbing effect of FX on the oral glucose tolerance test suggested the involvement of accelerated glycolysis and, more likely, of intestinal malabsorption.

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Effect of Cycloheximide on the Cell Cycle of the Crypts of the Small Intestine of the Rat

Cited by 74 publications

References 41 publications

Inhibitory Effect of Nivalenol, a Toxic Metabolite of Fusarium Nivale, on the Growth Cycle and Biopolymer Synthesis of Hela Cells

Inhibitory Effect of Nivalenol, a Toxic Metabolite of Fusarium Nivale, on the Growth Cycle and Biopolymer Synthesis of Hela Cells

Cell death: Apoptosis versus necrosis (Review)

Hypoglycemia in Mice Administered With Fusarenon-X

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