Document badmK4mEeGJ5G1BqZe4aYRgkD

^/ALOG ALERT DA001 User:0O4736 15jan92 PR 49/7/1 150 (Items f-44) DIALOG Alert PRINTS for 00*9202 Item PAGE: 23 Of lO 44 DIALOG File 154: MEDLINE _ 85-92/FEB (9202) chang d In various brain regions. It is concluded that this Investigation failed to reveal overt toluene-Induced CNS-neurotox1c1ty, however, certain Irreversible effects were found which further add to the accumulating evidence of the chronic CNS-neurotoxlefty of toluene. 07912002 92050002 Neurotoxicity of ammonia and fatty acids: differential Inhibition of mitochondrial dehydrogenases by ammonia and fatty acyl coenzyme A derivatives. Lai JC: Cooper AJ Department of Biochemistry, Cornell University Medical Coll g . New York, NY 10021. N urochern Res (UNITED STATES) Jul 1991, 16 (7) p795-803, ISSN 0364-3190 Journal Code: NX9 Contract/Grant No.: NS 24592; DK 16739 Languages: ENGLISH Document type: JOURNAL ARTICLE In several metabolic encephalopathies, hyperammonemia and rganlc acfdemla are consistently found. Ammonia and fatty acids (FAs) are neurotoxic: previous workers have shown that mmonla and FAs can act singly. In combination, or synerglstlcalty. In Inducing coma In experimental animals. Howev r, the biochemical mechanisms underlying the neurotoxicity of ammonia and FAs have not been fully elucidated. FAs are normally converted to their corresponding CoA derivatives (CoAs) once they enter cells and it is known th t these fatty acyl CoAs can alter Intermediary metabolism. Th pres nt study was initiated to determine the effects of ammonia and fatty acyl CoAs on brain mitochondrial d hydrogenases. At a pathophysiological level (2 mM), ammonia is a potent Inhibitor of brain mitochondrial alpha-ketoglutarate dehydrogenase complex (KGDHC). Only at toxicological levels (10-20 mM) does ammonia Inhibit brain mttochondrlal NAD(+>- and NADP(+)- linked Isocitrate d hydrog nase (NAO-ICOH. NADP-ICDH), and NAD(+)-linked malate dehydrogenase (MDH) and liver mitochondrial NAO-ICDH. Butyryl- (BCoA), octanoyl- (OCoA), and palmitoyl (PCoA) CoA were potent inhibitors f brain mitochondrial KGDHC. with IC50 values of 11, 20, and 25 mlcroM, respectively; moreover, the Inhibitory eff ct of fatty acyl CoAs and ammonia were additive. At levels of 250 mlcroM or higher, both OCoA (IC50 * 1.15 mM) and PCoA (IC50 * 470 mlcroM) Inhibit brain mitochondrial NADP-ICDH; only at higher levels (0.5-1 mM) does BCoA Inhibit this enzyme (by 30-45)4). Much less sensitive than KGDHC and NADP-ICDH, brain mitochondrial NAD-ICDH Is only Inhibited by 1 mM BCoA, OCoA, and PCoA by 22%, 35%, and 44%, respectIvely.(ABSTRACT TRUNCATED AT 250 WORDS) ASI 00005024 07911433 92049433 The Influence of solvent stress on MMS-Induced genetic change In Saccharomyces cerevlslae. Zlmmermann FK; Rohtfs A Instftut fur Darmstadt, F.R.G. Mtkrobfologle. Technlsche Hochschule, 023082 Mutat Res (NETHERLANDS) Sep-Oct 1991, ISSN 0027-5107 Journal Code: NNA Languages: ENGLISH 250 (1-2) p239-49, Document type: JOURNAL ARTICLE MMS Induced mitotic recombination but not mttotlc chromosome loss when tested In pure form In strain D61.M of Saccharomyces cerevlslae, confirming previous results of Albertinl (1991), whereas In Aspergillus nldulans It also Induced chromosomal malsegregation In addition to mitotic recombination (Kafer, 1988). However, Induction of mitotic chromosome loss was observed In combination with strong Inducers of chromosom loss such as the aprotlc polar solvents ethyl acetate and to a lesser extent methyl ethyl ketone but not with gamma-valerolactone and proplonttrlie. In addition to this, 4 solvents, dimethyl formamlde, dimethyl sulfoxide, dioxane and pyridine, enhanced the MMS-Induced mttotlc recombination In strain D61.M. An enhancement of MMS-Induced mitotic recombination and reverse mutation could be demonstrated for ethyl acetate and gamma-valerolactone In yeast strain D7. (7sr-- o t - v- 07910879 92048879 [Vinyl chloride end hastanglosarcoma of the liver] Vlnylchlorld und Hamangtosarkom der Leber. von Schonfeld J; Breuer N Abtel lung fur Gastroenterologle, Med1z1n1schen Unlversltatsklinlk Essen. Med Klin (GERMANY) Sep 15 1991, 86 (9) p482-4, ISSN 0723-5003 Journal Code: M9K Languages: GERMAN Document type: JOURNAL ARTICLE: REVIEW; REVIEW, TUTORIAL (28 Refs.) 07910172 92048172 Inhibition of acetaminophen activation by ethanol and acetaldehyde In liver mlcrosomes. Sato C; Liu J; Mlyakawa H; Nouchi T; Tanaka Y; Uchthara M; Marumo F Division of Health Science. School of Allied Health Sciences, Tokyo Medical and Dental University, Japan. Life Scl (ENGLAND) 1991, 49 (24) p1787-91, ISSN 0024-3205 Journal Code: L62 Languages: ENGLISH Document type: JOURNAL ARTICLE Mechanisms of the inhibitory effect of ethanol on acetaminophen hepatotoxlclty are controversial. We studi d the effects of ethanol and acetaldehyde, an oxidative m tabol1te of ethanol, on NADPH-dependent acetaminophen-glutathione conjugate production In liver mlcrosomes. Ethanol at concentrations as low as 2mM prevented the conjugate production noncompetIttvely. Acetaldehyde elso inhibited acetaminophen-glutathione c njugate production at concentrations as 1 w as 0.1mM that Is comparable with thos observ d In vivo after social drinking. Acetaldehyde may be (cont. n xt page)