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PubMed1994

Species differences in the biotransformation of ethyl chloride. II. GSH-dependent metabolism.

Groups of male and female F-344 rats and B6C3F1 mice were exposed to 15,000 ppm ethyl chloride (monochloroethane, ECL) or to air for 5 days (6 h/day). In this report, features of GSH-dependent ECL metabolism in the animals are described. A concurrent report describes the features of the cytochrome P450-dependent oxidative ECL metabolism (Fedtke et al. 1994). ECL conjugation to GSH in hepatic cytosolic fractions was catalyzed by GSH S-transferases. The specific activities were 0.16 +/- 0.03 and 0.17 +/- 0.01 nmol ECL conjugated/(min mg protein) in air treated male and female F-344 rats, respectively. These activities were not significantly altered by the ECL treatment. Compared with rats, the GSH-transferase activities towards ECL were generally higher in male and female B6C3F1 mice (0.71 +/- 0.19 and 1.01 +/- 0.19, respectively) and were slightly decreased by ECL treatment. The ECL conjugation to GSH resulted in a marked reduction of the GSH concentration in the lung and the uterus after 5 days of exposure. In contrast, liver and kidney GSH concentrations were affected only to a minor degree. Formed S-ethyl-glutathione was converted to the mercapturic acid S-ethyl-N-acetyl-L-cysteine (SENACys), which was detected in the urine of both species. In addition, the non-acetylated intermediate S-ethyl-L-cysteine (SECys) was excreted in mouse urine but not in rat urine. The cumulative amounts of SENACys and SECys excreted after 5 days were up to fivefold higher in mice than in rats and the excretion kinetics were species specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1994

Species differences in the biotransformation of ethyl chloride. I. Cytochrome P450-dependent metabolism.

Groups of male and female F-344 rats and B6C3F1 mice were exposed to 15,000 ppm ethyl chloride (monochloroethane, ECL) or to air for 5 days (6 h/day). In this report, features of the P450-dependent ECL metabolism in the animals are described. A concurrent report describes the in vitro and in vivo features of the GSH-dependent ECL metabolism (Fedtke et al. 1994). ECL is oxidatively dechlorinated in an NADPH- and O2-dependent reaction, resulting in the formation of acetaldehyde (AC). The oxidative ECL metabolism rates in microsomal incubations were measured. The results indicated induction of the oxidative ECL metabolism by ECL itself in mice and female rats. The hydroxylation of p-nitrophenol, which was used as an indicator of P450IIE1 activity, was also induced in microsomal incubations from ECL-exposed mice and female rats, but, corresponding to the ECL metabolism, not in male rats. In contrast, catalytic activities related to P450IA and IIB subfamilies were not induced by ECL treatment. Additional experiments with the P450IIE1-specific inhibitor 3-amino-1,2,4-triazole and induction experiments with acetone, phenobarbital and methylcholanthrene confirmed that the isoenzyme mainly involved in the dechlorination reaction is cytochrome P450IIE1. AC was not detected in serum of ECL exposed animals and only slightly enhanced amounts were detected in urine samples from ECL exposed mice, reflecting the high capacities of the AC metabolizing pathways in vivo. The data are discussed with regard to the results of a 2-year bioassay with F-344 rats and B6C3F1 mice exposed to 15,000 ppm ECL (NTP 1989a).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1989

Ethyl chloride: 11-day continuous exposure inhalation toxicity study in B6C3F1 mice.

Groups of seven B6C3F1 mice per sex were exposed for 23 hr/day to 0, 250, 1250, or 5000 ppm ethyl chloride (EtCl) for 11 consecutive days to evaluate the potential toxicity of EtCl under near-continuous exposure conditions. On the day following the last exposure, a neurobehavioral observation battery was performed, samples were obtained for clinical chemistry and hematology, and necropsies were conducted. Histopathologic examination was subsequently performed. The only observed effects were increased relative liver weights and a slight increase in hepatocellular vacuolation (glycogen or fat) in 5000 ppm-exposed mice. Exposures to EtCl were well tolerated despite the unusually long exposure periods.

Administration, Inhalation↗
PubMedDate not supplied

Ethyl chloride: a two-week inhalation toxicity study and effects on liver non-protein sulfhydryl concentrations.

Male and female Fischer 344 rats (6/sex/exposure concentration) and male beagle dogs (2/exposure concentration) exposed to 0, 1600, 4000 or 10 000 ppm ethyl chloride (EtCl) for 6 hr/da, 5 da/wk for 2 weeks showed no toxicologically significant treatment-related effects on body weights; clinical chemistry, hematology, or urinalysis parameters; neurology (dogs only were examined); gross pathology or histopathology. The only treatment-related differences in organ or relative organ weights (in rats or dogs) were slight, but statistically significant increases in liver to body weight ratios of male rats exposed to 4000 or 10,000 ppm EtCl (4.9 and 7.5% respectively). Liver non-protein sulfhydryl (NPSH) concentration was measured in male Fischer rats and male B6C3F1 mice that were exposed for 6 hours to 0, 1600, 4000 or 10,000 ppm EtCl (mice were exposed to 0 or 4000 ppm EtCl only). Liver NPSH, measured 1/2 hr post exposure, was less than control values in 4000 ppm exposed rats (88% of control value), 4000 ppm exposed mice (64%), and 10,000 ppm exposed rats (89%). The slight decreases in rat liver NPSH seem consistent with the increased liver to body weight ratios. The toxicity data indicate that 2-week repeated exposures to EtCl concentrations that were up to 10 times the current A.C.G.I.H. T.L.V. (1000 ppm) caused minimal treatment-related effects in dogs and rats.

Animals↗
PubMed1976

Allergic contact dermatitis from propellants in deodorant sprays in combination with allergy to ethyl chloride.

Allergic contact eczema from the use of deodorant sprays is sometimes caused by sensitization to the propellants. Positive reactions were seen in three patients when patch testing to Freon 11 (trichloromonofluoromethane). One patient also reacted to Freon 12 (dichlorofluoromethane). Another patient had an eczematous eruption after ethyl chloride was sprayed on the skin prior to taking biopsy. The two other patients showed strongly positive patch tests with this compound. Further investigations of the sensitizing capacity propellants with chemical resemblance have to be carried out to solve the problem of cross-sensitization.

Adult↗
PubMed1995

Analgesia for venous cannulation: a comparison of EMLA (5 minutes application), lignocaine, ethyl chloride, and nothing.

Three commonly available local anaesthetics were compared, in a controlled trial, for use before venous cannulation. The pain of application of the local anaesthetic, the pain of cannulation, and the rate of successful cannulations were compared. The value of EMLA cream applied for 5 min was questioned. Venous cannulation with a 20G venflon was found to be significantly more painful than the application of any of the local anaesthetics (P < 0.01). Lignocaine 1%, injected subcutaneously, and ethyl chloride spray significantly reduced the pain of venous cannulation (P < 0.01). The use of lignocaine did not result in significantly more failed cannulations than the control group. It was concluded that local anaesthesia should be used before venous cannulation, even for 20G cannulae.

Adult↗