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PubMed1983

Ultimate forms of mutagenic and carcinogenic heterocyclic amines produced by pyrolysis.

A mutant strain of Salmonella typhimurium TA98/1,8-DNP6 isolated by McCoy et al. (1) was reported to be defective in esterifying activity. We have found that 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1), 2-aminodipyrido[1,2-a:3',2'-d]imidazole (Glu-P-2), 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ), 2-amino-3,4-dimethylimidazo[4,5-f]quinoline (MeIQ) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) were not mutagenic to TA98/1,8-DNP6 with S9 mix, while these compounds were strongly mutagenic to the original TA98 with S9 mix. The mutagenicities of some of these heterocyclic amines to TA98 were inhibited by pentachlorophenol, an aryl sulfotransferase inhibitor. These results indicate that the ultimate forms of these heterocyclic amines are probably sulfate esters of heterocyclic amine N-hydroxides. Contrary to this, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), 2-amino-9H-pyrido[2,3-b]indole (A alpha C) and 2-amino-3-methyl-9H-pyrido[2,3-b]indole (MeA alpha C) were definitely mutagenic to TA98/1,8-DNP6, although less than to TA98.

Amines↗
PubMed1991

Formation of trisaccharides (kestoses) by pyrolysis of sucrose.

Amorphous sucrose, containing citric acid as catalyst, undergoes thermolysis at 100 degrees to yield fructofuranosyl cation and D-glucose. The cation reacts with unchanged sucrose to form all three of the known kestoses, and also their alpha-fructofuranosyl anomers. Two of the latter are resistant to invertase hydrolysis. A new fructosylglucose disaccharide is also formed.

Carbohydrate Sequence↗
PubMed1980

Myeloperoxidase-catalyzed binding of 3-amino-1-methyl-5H-pyrido[4,3-b]indole, a tryptophan pyrolysis product, to protein.

Incorporation of 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), the principal mutagen in a tryptophan pyrolysate, into bovine serum albumin was catalyzed by myeloperoxidase. Hydrogen peroxide was essential for the incorporation reaction and albumin was required for optimal incorporation of Trp-P-2 into protein. Other various proteins, such as histone, lysozyme, cytochrome c, and gamma-globulin could also incorporate Trp-P-2, but poly(L-Arg), poly(L-Lys), and poly(L-Glu) could not. The incorporation of Trp-P-2 into albumin was inhibited by L-tyrosine and L-tryptophan, but not by other amino acids. Trp-P-2 incorporated into albumin was not released from the protein by treatment with 0.3 N HCl, or 0.3 N NaOH for 2 h at 35 degrees C, or with 1% sodium dodecylsulfate for 2.5 min at 100 degrees C. On electrophoresis on polyacrylamide containing sodium dodecylsulfate or urea and on chromatography on Sepharose CL-6B in 6 M guanidine/HCl, Trp-P-2 incorporated into albumin or lysozyme migrated with these proteins. These findings indicate that Trp-P-2 is covalently bound to these acceptor proteins.

Albumins↗
PubMed1982

Pharmacological activity and toxicity of phencyclidine (PCP) and phenylcyclohexene (PC), a pyrolysis product.

Initial acute behavioral studies in mice indicated that phencyclidine (PCP) produced marked motor impairment as measured by the inverted screen technique with an ED50 value of 4.1 muMole/kg (i.v.). Phenylcyclohexene (PC) was considerably less active with an ED50 value of 325 muMole/kg (i.v.). PCP was also shown to be more lethal than PC as acute (24 hr; i.v. injection) LD50 values (muMoles/kg) in males were 57 and 448, and in females were /6 and 425, respectively. A greater acute lethality was also produced by PCP after i.p. and p.o. administration. Subchronic (14-day) exposure (i.p.) to PCP at doses up to approximately 40 percent of the acute LD50 value (123.6 muMole/kg, i.p., daily) was without significant effect on body and organ weights, hematology and clinical chemistry, and humoral and cell-mediated immunity. Higher doses of PCP were not possible because of acute lethality. Subchronic exposure to PC (63.4, 317, and 634.5 muMoles/kg; 4 percent, 20 percent and 40 percent of acute i.p. LD50 value, respectively) produced several marked effects. At the highest dose tested, body weight and thymus weight in both males and females, and liver weight in males were significantly decreased. The spleen weight of males exposed to 317 muMole/kg PC was also significantly decreased. Humoral immunity (production of antibody forming cells) was significantly inhibited in both males and females exposed to PC. In contrast, cell-mediated immunity (development of a delayed-type hypersensitivity response) was only significantly inhibited in females. As PCP has no measurable toxicity under these conditions and PC produced significant effects at relatively high doses, the results suggest that neither chemical is exceptionally toxic following subchronic exposure.

Animals↗
PubMed1983

Liver morphology in guinea pigs administered either pyrolysis products of a polychlorinated biphenyl transformer fluid or 2,3,7,8-tetrachlorodibenzo-p-dioxin.

A transformer cooled and insulated with a mixture of 65% Aroclor 1254 and 35% chlorinated benzenes located in the Binghamton State Office Building in Binghamton, New York, was involved in a fire, which produced soot containing polychlorinated biphenyls, biphenylenes, dioxins, and dibenzofurans. A single dose of either soot or 2,3,7,8-tetrachlorodibenzo-p-dioxin in aqueous methyl cellulose was administered by gavage to Hartley guinea pigs of both sexes. The liver tissue was examined 42 days after administration. By light microscopy hypertrophy of hepatocytes, steatosis, focal necrosis, and cytoplasmic hyalin-like bodies were observed as a result of both treatments. Bile duct proliferation (adenofibrosis) was observed only in the guinea pig groups administered soot. These animals also showed proliferation of the smooth endoplasmic reticulum, concentric membrane arrays (CMA), mitochondrial alterations, decreased rough endoplasmic reticulum, and autophagolysosomes by electron microscopy. The CMAs, which corresponded to the hyalin-like bodies, surrounded lipid droplets and cytoplasmic matrix containing mitochondria and degenerating organelles.

Animals↗
PubMed1984

Liver morphology in guinea pigs fed pyrolysis products of a polychlorinated biphenyl transformer fluid continuously for 90 days.

After a fire involving a transformer, the State Office Building in Binghamton, New York, was contaminated with soot containing polychlorinated biphenyls, biphenylenes, naphthalenes, dioxins, and dibenzofurans. The toxicity of the soot and its effect on liver morphology after prolonged (subchronic) exposure were determined for both sexes of Hartley guinea pigs, which were fed soot continuously for 90 days. By light microscopy the observed alterations of the liver were predominantly centrilobular; they included hepatocyte hypertrophy, steatosis, increased glycogen and iron, focal necrosis, and bile duct proliferation with fibrosis. Cytoplasmic vacuoles and acidophilic hyalin-like bodies were observed. Electron microscopy of hepatocytes showed proliferated smooth endoplasmic reticulum (SER), cytoplasmic vacuoles, concentric membrane arrays (CMAs), glycogen bodies, and microdroplets of fat, often without limiting membranes. The vacuoles frequently contained membrane fragments and had a halo-like periphery composed of proliferated membranes. Cell debris, membrane fragments, and small CMAs were observed in the sinusoids. Membrane fragments were also observed in the bile canaliculi and bile ducts. Intoxicated bile duct cells contained more cytoplasmic myelin whorls and altered mitochondria. In contrast to the previously reported study of a single dose, these liver alterations showed a strong dose dependence, emphasizing the importance of time and method of administration. The cytoplasmic vacuoles, which were not pronounced in the previous study, are here a prominent alteration, probably originating from outpouchings of canaliculi and sinusoidal membranes. A hypothesis for the mechanism of hepatocyte detoxification based on the proliferated SER and ejection of membrane fragments is proposed.

Animals↗