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There is increasing evidence that the mechanisms of chemically mediated cell death are common to a wide variety of cell types and to a large number of toxic compounds. The perturbation of Ca2+ homeostasis appears to be particularly important and may be due to modification of SH-groups in key enzymes. Donald Davies and colleagues discuss the mechanisms by(More)
Paracetamol is cytotoxic to hamster isolated hepatocytes by a mechanism that does not involve an early increase in [Ca2+]i. Although an increase in [Ca2+]i does occur, it accompanies rather than precedes, loss of viability. Studies with the ionophore, 4-bromo-A23187, suggest that although sustained elevations of [Ca2+]i per se can initiate cell death, this(More)
1 The ability of iloprost (ZK36374) to protect hamster isolated hepatocytes from the toxic effects of paracetamol and its reactive metabolite N-acetyl-p-benzoquinoneimine (NABQI) was investigated. The cytoprotection provided by iloprost was compared with that of N-acetyl-L-cysteine. 2 Treatment of hepatocytes with either NABQI (0.4 mM) or paracetamol (2 mM)(More)
Induced differentiation of cultured astrocytes to a process-bearing morphology has been described with a variety of agents known to increase intracellular cyclic AMP. The ionophores A23187 and ionomycin were found to induce a reversible change in astrocyte morphology to a process-bearing form. Cell death also occurs following exposure to either A23187 or(More)
In 1969 alpha-chlorohydrin was reported to have a reversible antifertility effect in male rats. It has since been reported to have a reversible antifertility effect in many other species but not in mice and rabbits. In chronic high-dosage regimens it was reported to be neurotoxic to mice. At high doses the 6-chloro-6-deoxysugars were found to have a(More)
In a previous paper we have shown that the calcium ionophores, A23187 and ionomycin, induce a morphological differentiation of cultured astrocytes to a process-bearing form. As A23187 is known to induce the turnover of inositol phospholipids in astrocytes, and this response is dependent on extracellular calcium, we examined the morphological effects of(More)
In a well-established two phase model of paracetamol toxicity in hamster hepatocytes cell death was accompanied, but not preceded, by a rise in cytosolic free calcium [Ca2+]i. Cell death appears to involve reversible oxidative damage, possibly to the cytoskeleton or mitochondria. In this model low concentrations (10(-8) to 10(-14) M) of iloprost, a stable(More)
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