PMID- 1733043
OWN - NLM
STAT- MEDLINE
DCOM- 19920227
LR  - 20190727
IS  - 0041-008X (Print)
IS  - 0041-008X (Linking)
VI  - 112
IP  - 1
DP  - 1992 Jan
TI  - Effect of methyl bromide on regional brain glutathione, 
      glutathione-S-transferases, monoamines, and amino acids in F344 rats.
PG  - 120-7
AB  - Both metabolic and neurotransmitter changes have been implicated in the 
      pathogenesis of monohalomethane neurotoxicity in rodents. This study in male and 
      female F344 rats examined the effects of methyl bromide (MeBr) on regional brain 
      glutathione-S-transferase (GST) activities and concentrations of glutathione 
      (GSH), monoamines, and amino acid. Inhalation exposure to 150 ppm MeBr (6 hr/day 
      x 5 days) yielded no histologic evidence of brain lesions but resulted in a 
      number of biochemical changes. GSH depletion and GST inhibition were detected in 
      the frontal cortex, caudate nucleus, hippocampus (examined for GSH only), brain 
      stem, and cerebellum from animals of both sexes. Differences between sexes were 
      detected for GSH depletion. Simultaneous treatment of rats with the inhibitor of 
      monohalomethane toxicity, BW 755C 
      (3-amino-1-[m-(trifluoromethyl)phenyl]-2-pyrazoline; 10 mg/kg bw ip, 1 hr pre- 
      and 1 hr postexposure) completely protected against GST inhibition in all brain 
      regions of both sexes. Partial protection by BW 755C against GSH depletion was 
      observed in the cerebral cortex and in the cerebellum only. In males, MeBr 
      exposure had no effect on the regional concentrations of the monoamines dopamine 
      and serotonin and the amino acids glutamate, glutamine, taurine, and 
      gamma-aminobutyric acid. Regional increases of brain aspartate and glycine levels 
      were observed after exposure of males to MeBr but BW 755C had no effect on these 
      changes induced by MeBr. Thus, of all the parameters studied, only GST, and in 
      some brain areas GSH, correlated with inhibition of toxicity. It is concluded 
      that, in contrast to the monoamines and the amino acids, GST and GSH are 
      sensitive and potentially relevant indicators of MeBr neurotoxicity which could 
      explain sex and regional differences in response to the monohalomethanes.
FAU - Davenport, C J
AU  - Davenport CJ
AD  - CIIT, Research Triangle Park, North Carolina 27709.
FAU - Ali, S F
AU  - Ali SF
FAU - Miller, F J
AU  - Miller FJ
FAU - Lipe, G W
AU  - Lipe GW
FAU - Morgan, K T
AU  - Morgan KT
FAU - Bonnefoi, M S
AU  - Bonnefoi MS
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Toxicol Appl Pharmacol
JT  - Toxicology and applied pharmacology
JID - 0416575
RN  - 0 (Amino Acids)
RN  - 0 (Biogenic Monoamines)
RN  - 0 (Hydrocarbons, Brominated)
RN  - 9V42E1Z7B6 (methyl bromide)
RN  - EC 2.5.1.18 (Glutathione Transferase)
RN  - GAN16C9B8O (Glutathione)
SB  - IM
MH  - Amino Acids/*metabolism
MH  - Animals
MH  - Biogenic Monoamines/*metabolism
MH  - Brain/*drug effects/*metabolism
MH  - Female
MH  - Glutathione/*metabolism
MH  - Glutathione Transferase/*metabolism
MH  - Hydrocarbons, Brominated/*pharmacology
MH  - Male
MH  - Rats
MH  - Rats, Inbred F344
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
AID - 10.1016/0041-008x(92)90287-3 [doi]
PST - ppublish
SO  - Toxicol Appl Pharmacol. 1992 Jan;112(1):120-7. doi: 10.1016/0041-008x(92)90287-3.