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EC number: 201-174-2
CAS number: 79-07-2
In vitro supporting data were available for Chloroacetamide, demonstrating a rapid drop in hepatocellular glutathione content, followed by lipid peroxidation, morphological changes and possible lysis of the treated cells. However during in vivo studies in rats, GSH depletion and morphological changes were demonstrated to be rapid and reversible within 24-48 hours, therefore Chloroacetamide led to rapid GSH depletion with possible lipid peroxidation however without permanent damage of hepatocytes.
Supporting studies were available on the effect of
Chloroacetamide on hepatic gluthatione (GSH). GSH is a co-factor for the
selenium dependent GSH-peroxidase, and is important in the defence
against lipid peroxidation. It has also become evident that GSH protects
against protein alkylation and that compounds that deplete GSH may
alkylate proteins, leading to cellular damage.
In an in vitro study, primary
rat hepatocytes obtained from Sprague-Dawley rats were incubated for 4
to 5 hours with serum to which 18.7 µg chloroacetamide/mL had been
added. There was a very sharp drop in
cellular glutathione content in the
first hour of incubation with Chloroacetamide, as well as a considerable
enhancement of lipid peroxidation and
marked lysis of the treated cells (Anundi et al., 1979). By adding
methionine, which stimulates hepatocellular
glutathione synthesis, it was possible to achieve clear inhibition of
all of the effects described.
Another study in male Sprague-Dawley rats investigated
the effect of chloroacetamide on lipid peroxidation in vivo by means of
the ethane/pentane breath test (Cluet & Boudène, 1983). Chloroacetamide
was administered intraperitoneally at dose levels of 70, 80 and 150
mg/kg body weight. Upon treatment, the animals were immediately placed
in closed breathing chambers with circulating air, and the amounts of
ethane and pentane exhaled over periods of 2 and 4 hours were measured.
Increases in the exhaled amounts of ethane and pentane were only small
at 4 hours after the 70 mg/kg body weight dose, marked at 4 hours after
the 80 mg/kg body weight dose and very marked at only 2 hours after the
150 mg/kg body weight dose. At the highest dose level, the animals died
after 2 hours. The authors therefore saw the findings of Anundi et al.
(1980) regarding chloroacetamide- induced stimulation of lipid
peroxidation in vivo confirmed by an independent method.
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