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Drug-Target Interaction

Drug

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PubChem ID:6850715
Structure:
Synonyms:
1,2-xylene
1,3-dimethylbenzene
1,3-xylene
1,4-xylene
AC1OA804
AI3-02209-X
Benzene, dimethyl-
BRN 1901563
Caswell No. 906
CCRIS 903
CID6850715
Dimethylbenzene
Dimethylbenzene (mixed isomers)
Dimethylbenzenes
EINECS 215-535-7
EPA Pesticide Chemical Code 086802
except p-xylene, mixed or all isomers
HSDB 4500
Ksylen [Polish]
LS-767
m & p-xylene
m-,p-,o-Xylene
Methyl toluene
Methyltoluene
mixed Xylenes
Mixed xylenes (m-xylene, p-xylene, o-xylene, and ethylbenzene)
MolPort-009-755-088
NCI-C55232
o-,m-,p-Xylene
o-xylene
RCRA waste no. U239
RCRA waste number U239
Socal aquatic solvent 3501
ST50406765
ST5406765
Total xylenes
UN 1307
Violet 3
Xiloli [Italian]
Xyle ne
Xylene
Xylene (mixed isomers)
Xylene (mixed)
Xylene (o,m,p isomers)
Xylene (o-, m-, p-isomers)
Xylene (o-,m-,p-)
Xylene mixture
Xylene mixture (60% m-xylene, 9% o-xylene, 14% p-xylene, 17% ethylbenzene)
Xylene mixture (m-xylene, o-xylene, p-xylene)
Xylene, (total)
XYLENE, ACS
Xylene, isomers
Xylene, mixed
Xylene, mixed isomers, pure
xylene, mixed or all isomers, except p -
xylene, mixed or all isomers, except p-
XYLENEHistological Grade
Xylenen [Dutch]
Xylenes
Xylenes (isomers and mixture)
XYLENES (MIXED)
Xylenes (o-, m-, p-isomers)
Xylenes mixed isomers
Xylenes, total
Xylol
Xylole [German]

Target

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Uniprot ID:CP2B1_RAT
Synonyms:
CYPIIB1
Cytochrome P450 2B1
P450-B
P450-LM2
P450-PB1 and P450-PB2
P450b
EC-Numbers:1.14.14.1
Organism:Rat
Rattus norvegicus
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

9101035
Chlorodibromomethane metabolism to bromide and carbon monoxide in rats.. D Pankow; B Damme; U Wünscher; K Bergmann (1997) Archives of toxicology display abstract
The chlorodibromomethane (CDBM) metabolites bromide and CO were analysed as bromide level in plasma and carboxyhaemoglobin (COHb) level in blood of rats, respectively. The mean basic levels of bromide in plasma of rats receiving vehicle were 0.075 +/- 0.036 mmol/l (n = 27). After administration of CDBM at 0.4, 0.8, 1.6, and 3.1 mmol/kg p.o., the mean bromide levels rose to maximal values that were higher by a factor 27, 48, 69, and 135, respectively. Bromide elimination was slow and the plasma level was significantly increased following repeated administration in comparison to a single administration of CDBM. The CDBM concentrations in blood and in fat tissue 6 h after the last of 7 administrations of 0.8 mmol CDBM/ kg p.o., once a day for 7 consecutive days, were significantly lower than 6 h after a single gavage of this CDBM dose. The mean normal level of 0.45 +/- 0.32% COHb in rats (n = 30) was significantly increased following oral CDBM uptake. Initially higher COHb levels were measured after 7 consecutive applications of 0.8 mmol/kg CDBM. After a single administration of CDBM the level of glutathione disulphide in the liver was significantly increased; this effect was reversible. The oxidative CDBM metabolism was influenced by the glutathione (GSH) concentration in the liver. The rate of COHb and bromide formation was decreased after GSH depletion due to pretreatment of rats with buthionine sulphoximine (BSO) and increased following enhancement of the GSH concentration due to pretreatment of the animals with butylated hydroxyanisole (BHA). CDBM is a substrate for cytochrome P-450 2E1 (CYP2E1), as demonstrated by the inhibition of bromide and COHb formation due to simultaneous administration of CDBM and the CYP2E1 inhibitor diethyldithiocarbamate (DDTC); also by the initially higher levels of bromide in plasma and COHb in blood after gavage of CDBM pretreated with isoniazid (INH), an inducer of CYP2E1. The increase of bromide formation after CDBM administration in phenobarbital (PB)-pretreated rats indicated that cytochrome P-450 2B1 and 2B2 (CYP2B1 and CYP2B2) play a role as catalysts of the CDBM biotransformation. It is shown that m-xylene pretreatment, which activates CYP2E1 as well as CYP2Bs, leads to a higher bromide level after CDBM administration than the INH or PB pretreatment. In liver microsomes of rats treated with CDBM (0.8 mmol/kg p.o., seven daily applications), the p-nitrophenol hydroxylase (p-NPH) activity, a market of CYP2E1, was increased. It is concluded that CDBM may be an inducer of CYP2E1. These results combined with literature data demonstrate that the oxidation of CDBM was catalysed mainly by CYP2E1 and CYP2Bs and that there may be a risk of bromide accumulation following repeated uptake of the trihalomethane.