摘要:

Rats or mice developed centrolobular hepatic necrosis within 24 h after an intraperitoneal injection of 14C-bromobenzene or other radiolabeled halogenated aromatic hydrocarbons. The hepatic necrosis was preceded by the cova lent binding of substantial amounts of radiolabeled material to liver proteins, and autoradiograms revealed that most of the covalently bound material was localized within the necrotic centrolobular hepatocytes. Prior induction of hepatic microsomal enzymes by phenobarbital administration potentiated the covalent binding and necrosis, whereas prior inhibition of hydrocarbon metabolism had the opposite effects, suggesting that the binding and necrosis are caused by toxic metabolites of the hydrocarbons. These results imply that covalent binding of toxic metabolites may be an important mechanism in the pathogenesis of tissue lesions elicited by a variety of foreign compounds.

ISSN:0031-7012    

DOI:10.1159/000136440

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000135418

出版商:S. Karger AG    

年代:1964

数据来源: Karger

摘要:

By using drugs which alter the levels ofserotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) and norepinephrine (NE), we have shown that they effecttryptophan hydroxylase activity in the CNS. Relatively high doses of 5-HIAA and NE added in vitro also inhibittryptophan hydroxylase. The possibility that brain serotonin biosynthesis is regulated via an end-product feedback control mechanism is discussed.

ISSN:0031-7012    

DOI:10.1159/000136441

出版商:S. Karger AG    

年代:1973

数据来源: Karger

摘要:

The study of steroid metabolism by the hepatic microsomal enzymes is particularly useful since it provides an estimation of changes of a number of independent hydroxylases as well as reductase. This paper presents a simplified procedure for looking at the metabolism of testosterone by microsomal enzymes and further demonstrates its utility as an approach for examining the effect of parathion on testosterone metabolism.

ISSN:0031-7012    

DOI:10.1159/000136442

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000135419

出版商:S. Karger AG    

年代:1964

数据来源: Karger

摘要:

The activity of amantadine HCl, trihexyphenidyl HCl, ethopropazine HCl, atropine sulphate, mecamylamine HCl and L-dopa against effects provoked by nicotine injected intracerebrally(tremors, convulsions, loss of righting reflex) was studied. The antagonistic drugs were injected intraperitoneally or intracerebrally.The above mentioned drugs except L-dopa and atropine preventednicotine manifestations when given intraperitoneally. Amantadine, atropine and mecamylamine, resulted active when given intracerebrally (trihexyphenidyl, ethopropazine and L-dopa could not betested i.e.). Effects provoked by oxotremorine were counteracteby atropine, trihexyphenidyl, ethopropazine but not by amantadineand mecamylamine. Trihexyphenidyl, ethopropazine and atropine had anticarbamylcholine activity and mydriatic activity. Amantadine and mecamylamine were inactive or almost inactive.

ISSN:0031-7012    

DOI:10.1159/000136443

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000135420

出版商:S. Karger AG    

年代:1964

数据来源: Karger

摘要:

The anticataleptic activity of amphetamine, phenmetrazine, cocaine, apomorphine, yohimbine, and L-dopa wasdetermined in mice. Cataleptic states were produced using haloperidol, trifluoperazine, pilocarpine, nicotine, paraoxon, and tetrabenazineIn general, the anticataleptic activities of amphetamine, phenmetrazine, cocaine and yohimbine were of the same order of magnitude, nicotine catalepsy being preferentially antagonized by am hetamine and yohimbine. L-dopa was anticataleptic only when theanimals were pretreated with a monoamine oxydase inhibitor(iproniazid), but failed to antagonize the trifluoperazine catalepsy.Apomorphine exhibited very weak anticataleptic activity and was completely inactive against nicotine catalepsy.

ISSN:0031-7012    

DOI:10.1159/000136444

出版商:S. Karger AG    

年代:1973

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000135421

出版商:S. Karger AG    

年代:1964

数据来源: Karger

ISSN:0031-7012    

DOI:10.1159/000135422

出版商:S. Karger AG    

年代:1964

数据来源: Karger