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PubMed1987

Peroxisome induction studies on seven phthalate esters.

Seven phthalate esters, representing a variety of chain lengths and degrees of branching in the alcohol moiety, were tested for their ability to produce peroxisome proliferation in the Fischer 344 rat. Di(2-ethylhexyl)adipate (DEHA) was tested using the same protocol and di(2-ethylhexyl)phthalate (DEHP) was run with each study as an internal control. Each ester was administered in the feed for a period of 21 days at levels of 2.5%, 1.2% and either 0.6% or 0.3%. DEHP and DEHA were also fed at levels of 0.1% and 0.01%. The animals were sacrificed and samples of liver were prepared for both light and electron microscopy. Serum samples were assayed for both triglyceride and cholesterol. The remaining portion of the liver was homogenized and assayed for cyanide-insensitive palmitoyl-CoA oxidation, lauric acid 11-hydroxylase and lauric acid 12-hydroxylase. The results show that there is approximately a ten-fold difference between the weakest and strongest esters in terms of their potency to induce changes in relative liver weight and in several of the biochemical parameters. In general, the longer chain esters were more potent than the shorter chain ones, and branched chain esters seemed more potent than straight. Several statistical analyses of the dataset have been performed and all render similar conclusions. The results of one of these evaluations are presented elsewhere in this volume (Lin, 1987).

Animals↗
PubMed1987

The use of multivariate analysis to compare peroxisome induction data on phthalate esters in rats.

This paper contains statistical evaluations of the effect of 9 different plasticizers on rat hepatic peroxisome proliferation. There were 9 21-day feeding studies with one plasticizer in each study. The plasticizers are: di(2-ethylhexyl)phthalate (DEHP), butyl benzyl phthalate (BBP), 711 phthalate (711P), di(n-butyl)phthalate (DBP), di(undecyl)phthalate (DUP), di(isodecyl)phthalate (DIDP), di(isononyl)phthalate (DINP), 610 phthalate (610P), and di(ethylhexyl)adipate (DEHA). For each plasticizer, several dosage (as % of diet) groups, plus a negative control group (0%) and a reference control group (1.2% DEHP) were included. There were 5 males and 5 females, approximately 5 weeks old, per group per plasticizer, for a total of 470 animals. For each animal, body weight and food intake were measured prior to treatment and twice a week during the treatment period. Animals were necropsied at the end of the 21-day treatment period. Selected organs and blood samples of each animal were collected for measuring hepatic enzymes, proteins, fat stains, organ weights and serum fats. The endpoints included electron microscopy examination of liver peroxisome proliferation and liver histological abnormalities. The statistical evaluation utilized a multivariate approach that condensed a complex phenomenon into certain meaningful and simple endpoints for quantitative comparisons. The dose of each plasticizer that would protect 99% and 99.9% of rats against peroxisome proliferation (xx% statistically predicted dose, or xx% SPD) was estimated. Marked differences were seen in the ability of the 9 test compounds to cause hepatic peroxisome proliferation in rats. The graphic ranking of overall potency is, in order from most potent to least potent: DEHP, DIDP, DINP, DBP, DEHA, DUP, BBP, 711P and 610P. The ranking in terms of 99.9% SPD is: DEHP, DINP, DIDP, DBP, 610P, DUP, DBP, 711P and DEHA. It was also found that the histological findings of reduced basophilia or increased eosinophilia were highly correlated with peroxisome proliferation (r = 0.94). The other histological findings were incidental observations for specific plasticizers.

Analysis of Variance↗
PubMed1987

Studies by the National Toxicology Program on di(2-ethylhexyl)phthalate.

In a 2-year feed study previously reported by the National Toxicology Program (NTP), the plasticizer di(2-ethylhexyl)phthalate (DEHP) was found to produce increased incidences of hepatocellular neoplasms in both sexes of Fischer 344 (F344) rats and B6C3F1 mice. Further studies by the NTP on this chemical have investigated its genotoxicity, dermal absorption, reproductive and developmental toxicity, and biochemical mechanism of action. DEHP was not mutagenic in Salmonella typhimurium (strains TA98, TA100, TA1535 or TA1537), in L5178Y mouse lymphoma cells, or in Drosophila melanogaster. DEHP did not induce chromosomal aberrations, but did cause a marginal dose-related increase in sister chromatid exchanges in CHO cells. In a dermal absorption study, DEHP was not absorbed well through the skin of F344 rats. In a fertility assessment study, DEHP was shown to be a reproductive toxicant in both male and female CD-1 mice. The teratogenic potential of DEHP was evaluated in F344 rats and CD-1 mice. In the rat study, there were no significant differences in percent fetuses malformed between control and treatment groups, even at dose levels (1.0, 1.5 and 2.0%) which produced significant maternal and fetal toxicity. In the mouse study, the incidence of fetuses with malformations was significantly increased at dose levels which produced maternal and/or fetal toxicity (0.10 and 0.15%), and at a dose level (0.05%) which did not cause maternal or fetal toxicity. The no-observed effect level for developmental toxicity in mice was 0.025% DEHP. Kinetic data on the rates of formation of H2O2 by peroxisomal palmitoyl CoA oxidase, and of degradation of H2O2 by catalase, was used to estimate in vitro steady-state H2O2 concentrations during peroxisomal oxidation of palmitoyl CoA. Increases in steady-state H2O2 in liver homogenates of rats treated with DEHP, di(2-ethylhexyl)adipate, or nafenopin, a hypolipidemic drug, correlated well with the carcinogenic potential of these chemicals determined in previous carcinogenicity studies, and are consistent with but not definitive evidence for the involvement of peroxisome proliferation in the hepatocarcinogenesis of these compounds.

Abnormalities, Drug-Induced↗
PubMed1993

Immunohistochemical localization of carboxylesterase in the nasal mucosa of rats.

The enzymatic esterase activity of carboxylesterases is integral to the nasal toxicity of many esters used as industrial solvents or in polymer manufacture, including propylene glycol monomethyl ether acetate, dimethyl glutarate, dimethyl succinate, dimethyl adipate, and ethyl acrylate. Inhalation of these chemicals specifically damages the olfactory mucosa of rodents. We report the localization and differential distribution of a 59 KD carboxylesterase in nasal tissues of the rat by immunohistochemistry. Rabbit antiserum against the 59 KD rat liver microsomal carboxylesterase bound most prominently to the olfactory mucosa when applied to decalcified, paraffin-embedded sections of rat nasal turbinates. Within the olfactory mucosa, anti-carboxylesterase did not bind to sensory neurons, the target cell for ester-initiated toxicity; these cells apparently lack carboxylesterase. Instead, the antibody was preferentially bound by cells of Bowman's glands and sustentacular epithelial cells which are immediately adjacent to the olfactory nerve cells. In contrast, non-olfactory tissues (respiratory mucosa and squamous epithelium), which are more resistant to the toxicity of esters, had less carboxylesterase content. The distribution of immunoreactivity correlated well with the distribution of carboxylesterase catalytic activity described elsewhere. These findings help to link the metabolic fate of inhaled esters to the site-specific pathological findings that follow exposure to such chemicals.

Animals↗
PubMed1982

C6-C10-dicarboxylic aciduria: investigations of a patient with riboflavin responsive multiple acyl-CoA dehydrogenation defects.

The abnormal metabolites-adipic, suberic, and sebacic acids-were detected in large amounts in the urine of a boy during a Reye's syndrome-like crisis. Substantial amounts of 5-OH-caproic acid, caproylglycine, glutaric acid, and 3-OH-butyric acid and moderately elevated amounts of ethylmalonic acid, methylsuccinic acid, 3-OH-isovaleric acid, and isovalerylglycine were also found. These metabolites were consistently present in urine samples collected in the boy's habitual condition after the attack. 1-[14C]-Palmitic acid was oxidized at a normal rate, whereas U-[14C]-Palmitic acid was oxidized at a reduced rate in cultured skin fibroblasts from the patient, thus indicating a defect at the level of medium- and/or short-chain fatty acid oxidation. Riboflavin medication (100 mg three times a day) significantly reduced the excreted amounts of pathologic metabolites, suggesting a flavineadeninedinucleotide-related acyl-CoA dehydrogenation defect as the cause of the disease. Carnitine in plasma was low in the patient (6 mumole/liter, controls 26-74 mumole/liter), suggesting carnitine deficiency as a secondary effect of the acyl-CoA dehydrogenation deficiency. The present patient, who presented with a Reye's syndrome-like attack, suffers from impaired dehydrogenation of acyl-CoA resulting in accumulation of acyl-CoA in the cells. Attacks with similar symptoms are seen in other acyl-CoA dehydrogenation deficiencies, such as glutaric aciduria types I and II, other types of C6-C10-dicarboxylic acidurias and isovaleric acidemia. Reduced flow through the acyl-CoA dehydrogenation steps may therefore be an ethiologic factor in Reye's syndrome. Several of the accumulated acyl-CoA's are toxic and may be responsible for some of the symptoms. The low carnitine level in plasma and the elevated esterified carnitine excretion in the present patient indicate that acyl-CoA accumulation may cause a functional carnitine deficiency by sequestration of carnitine as acyl-carnitines. As the inborn defect, systemic carnitine deficiency may exhibit symptoms like those of Reye's syndrome, it may be speculated whether functional carnitine deficiency in patients with accumulated acyl-CoA is another causal factor in the development of the symptoms during attacks.

Acyl Coenzyme A↗
PubMed1983

Episodic hypoglycemia with psi-hydroxy fatty acid excretion.

We present case histories of two young children with episodes of hypoglycemia, elevation of SGOT, low insulin levels, increased urinary excretion of psi-hydroxy fatty acids (5-hydroxyhexanoic, 7-hydroxyoctanoic and 9-hydroxydecanoic), traces of the corresponding psi-ketoacids and elevations of urinary adipic, suberic, and sebacic acids. The ratio of psi-hydroxy fatty acids to 3-hydroxybutyric in the urine of these patients is higher than in patients of similar ages with similar illnesses. These acids persisted while the patients were well. Increased urinary psi-hydroxy fatty acids could be reproduced by a load of medium chain triglycerides without precipitating other clinical symptoms. Three children with hypoglycemia were found not to excrete measurable amounts of these unusual acids while ill. A medium chain triglyceride load in one of these children after recovery failed to elicit psi-hydroxy acid excretion. Small amounts of urinary 5-hydroxyhexanoic acid only were found in two patients with acute Reye's syndrome and in three of five severely ill children with starvation ketonuria. In this last group, no urinary psi-hydroxyacids could be detected after recovery. Normal children do not excrete measurable amounts (less than 1 mg/g creatinine) of these psi-hydroxyacids.

Aspartate Aminotransferases↗
PubMed1986

Excretion of dicarboxylic and omega-1 hydroxy fatty acids by low birth weight infants fed with medium-chain triglycerides.

The effects of feeding a commercial formula containing increased amounts of medium-chain fatty acids on the urinary excretions of C6-C10 moncarboxylic, dicarboxylic, and omega-1 hydroxy acids were studied in 13 growing preterm infants of mean birth weight 1.42 kg in a randomized double-blind cross-over clinical trial. Infants were allocated to two sequential feeding regimes of 5 days each, during the last 3 days of which urine was collected and analysed by gas-chromatography mass spectrometry. The two feeding regimes consisted of high energy and protein-containing formulas specially designed for growing low birth weight infants. In one diet the triglyceride component consisted of 46% medium-chain (C8-C10) and 54% long-chain fatty acid residues: in the other it consisted of 4% medium-chain and 96% fatty acid residues. The infants were randomized so that six infants were fed first with the medium-chain predominant formula and seven were fed first with the long-chain predominant formula. There were significant differences in the urinary excretions of octanoate, sebacate, suberate, adipate, 7-hydroxyoctanoate, and 5-hydroxyhexanoate; these substances appearing in much greater quantities in the urine during the period in which medium-chain triglycerides were predominant in the formula. The significance of this organic aciduria, which accounted for 0.7% of the dietary intake of medium-chain triglycerides, remains to be established.

Dicarboxylic Acids↗
PubMed1987

Clinical and biochemical variation and family studies in the multiple acyl-CoA dehydrogenation disorders.

We report clinical and biochemical studies in patients with multiple acyl-CoA dehydrogenation disorders (MAD) and their parents. A severely affected (MAD:S) patient presented with neonatal acidosis leading to death and excreted a wide range of straight- and branched-chain acyl CoA derivatives. Two patients with mild variants of the same disorder (MAD:M) presented with neurologic abnormalities, acidotic coma, and/or poor growth; they primarily excreted ethylmalonate and variable amounts of adipate. Fibroblasts from the MAD:S patient demonstrated severely defective radiolabeled substrate oxidation, while the MAD:M cells had milder oxidative defects. Fibroblasts from two other MAD:M and six other MAD:S patients demonstrated analogous defects in substrate oxidation. As a group, MAD:S cells deficient in electron transfer flavoprotein:ubiquinone oxidoreductase had significantly lower residual oxidative activities than did MAD:S cells deficient in electron transfer flavoprotein. Fibroblasts from the parents of four MAD:S patients oxidized radiolabeled substrates significantly less effectively than did normal infant controls but were indistinguishable from normal adult cells. We found relatively higher residual oxidative activities in maternal than in paternal cells. Amniocytes from a fetus at risk for MAD:S catabolized labeled substrates normally; the infant has been clinically and biochemically normal up to 30 months of age.

Acyl-CoA Dehydrogenase↗
PubMed2006

Effects of possible endocrine disrupting chemicals on bacterial component-induced activation of NF-kappaB.

Endocrine disrupting chemicals (EDCs) have a possibility to exacerbate infectious diseases because EDCs disturb the human immune system by interfering with endocrine balance. To assess the influence of EDCs on the innate immune function of macrophages, we investigated the effects of thirty-seven possible endocrine disruptors on lipopolysaccharide (LPS)- or bacterial lipopeptide (Pam3CSK4)-induced activation of nuclear factor kappa B (NF-kappaB). Alachlor, benomyl, bisphenol A, carbaryl, kelthane, kepone, octachlorostyrene, pentachlorophenol, nonyl phenol, p-octylphenol and ziram inhibited both LPS- and Pam3CSK4-induced activation of NF-kappaB. Simazine inhibited only LPS-induced activation. A strong inhibitory effect was observed with ziram and benomyl. On the other hand, diethylhexyl adipate and 4-nitrotoluene tended to enhance the activation induced by Pam3CSK4 and LPS, respectively. Aldicarb, amitrole, atrazine, benzophenone, butyl benzyl phthalate, 2,4-dichlorophenoxy acetic acid, dibutyl phthalate, 2,4-dichlorophenol, dicyclohexyl phthalate, diethylhexyl phthalate, diethyl phthalate, dihexyl phthalate, di-n-pentyl phthalate, dipropyl phthalate, malathion, methomyl, methoxychlor, metribuzin, nitrofen, permethrin, trifluralin, 2,4,5-trichlorophenoxyacetic acid and vinclozolin had no significant effects at 100 microM. These results indicate that some agrochemicals have the potential to inhibit macrophage function and suggest that endocrine disruptors may influence the development of bacterial infections.

Animals↗
PubMed1992

[Synthesis of new antirusty disinfectants. I].

New quaternary ammonium salts [N-alkyl-N-2-hydroxyethyl-N,N-dimethylammonium ethyl phosphate (21, 22), isopropyl phosphate (23), n-butyl phosphate (24) and N-alkyl-N-2-hydroxy-3-phenoxypropyl-N,N-dimethylammonium ethyl phosphate (25, 26), isopropyl phosphate (27), n-butyl phosphate (28) and bis(N-alkyl-N-2-hydroxy-3-phenoxypropyl-N,N-dimethylammonium) malate (29), fumarate (30), succinate (31), adipate (32) and N-alkyl-N-2-hydroxy-3-phenoxypropyl-N,N-dimethylammonium tartrate (33)] were synthesized by alkylation of the corresponding trialkylammonium salts with various epoxy compounds. The new quaternary ammonium salts showed much greater bactericidal activities and antirusting effects than those of benzalkonium chloride. They had also good compatibilities since no precipitate was observed if the solution of any anionic surface active agents were added to the solution of these new quaternary ammonium salts. This property is the same as that of amphoteric surface active agents.

Bacteria↗
PubMed2002

Cloning and sequence analysis of poly(tetramethylene succinate) depolymerase from Acidovorax delafieldii strain BS-3.

A gene encoding poly(tetramethylene succinate), PBS, depolymerase, pbsA, has been cloned from Acidovorax delafieldii strain BS-3 chromosomal DNA. The clone expressed in Escherichia coli showed the ability to degrade both PBS and poly[(tetramethylene succinate)-co-adipate] that are kinds of biodegradable plastics. PBS depolymerase was considered to be a kind of lipase, since it also degrades olive oil. It had no apparent hydrophobic-amino-acid-rich region which exists in other known plastic-degrading enzymes. From the result of amino acid homology search, PbsA was found to have some similarities with lipases of Streptomyces sp. and Mollaxella sp. In the motif surrounding the active site Ser residue (Gly-X1-Ser-X2-Gly), PbsA was revealed to have a Trp residue in the X1 position instead of His which is most likely found in other bacterial lipases.

Journal Article↗
PubMed1993

Transformation of BALB/c-3T3 cells: IV. Rank-ordered potency of 24 chemical responses detected in a sensitive new assay procedure.

This report introduces an improved method of detecting chemical-induced morphological transformation of A-31-1-13 BALB/c-3T3 cells. The new procedure uses an increased target cell population to assess chemical-induced damage by increasing the initial seeding density and by delaying the initiation time of chemical treatment. Furthermore, a newly developed co-culture clonal survival assay was used to select chemical doses for the transformation assay. This assay measured the relative cloning efficiency (RCE) of chemical treatments in high-density cell cultures. In addition, transformation assay sensitivity was enhanced through the use of improved methods to solubilize many chemicals. From a group of 24 chemicals tested in at least two trials, clear evidence of chemical-induced transformation was detected for 12 chemicals (aphidicolin, barium chloride-2H2O, 5-bromo-2'-deoxyuridine, C.I. direct blue 15, trans-cinnamaldehyde, cytosine arabinoside, diphenylnitrosamine, manganese sulfate-H2O, 2-mercaptobenzimidazole, mezerein, riddelliine, and 2,6-xylidine); 2 chemicals had equivocal activity [C.I. direct blue 218 and mono(2-ethylhexyl)phthalate], 9 chemicals were inactive [carisoprodol, chloramphenicol sodium succinate, 4-chloro-2-nitroaniline, C.I. acid red 114, isobutyraldehyde, mono(2-ethylhexyl)adipate, sodium fluoride, and 12-O-tetradecanoylphorbol-13-acetate), and 1 chemical had an indeterminate response (2,6-dinitrotoluene). All positive responses were detected in the absence of an exogenous activation system and exhibited significant activity at two or more consecutive doses. This report also presents a mathematical method that uses t-statistics for rank-ordering the potency of chemical-induced transformation responses. This model detects sensitivity differences in experiments used to evaluate chemical-induced transformation. Furthermore, it provides a method to estimate a chemical's transformation response in terms of the historical behavior of the assay, as well as its future activity. The most active of the 24 chemicals was mezerein, and the least active chemical was diphenylnitrosamine.

3T3 Cells↗
PubMed2002

Plasma free amino acids in Taiwan Chinese: the effect of age.

Values of plasma amino acids (AA) in Taiwan Chinese in different age groups were determined. AA analysis was performed by ion-exchange chromatography. The results correlated well with the reference values published by Shapira in 1989, indicating that plasma AA concentrations are not evidently affected by race and dietary habits. We also confirmed the effect of age on plasma free AA levels. More than two thirds of 35 amino acids showed statistically significant differences between age groups (p<0.05, one-way ANOVA test). Levels of taurine, hydroxyproline, threonine, serine, glutamic acid, proline, citrulline and alpha-amino-eta-butyric acid varied with age (p<0.01). Only a few AA, including alpha-amino-adipic acid, glycine, alanine, cystine, homocystine, isoleucine, tyrosine, gamma-aminobutyric acid and tryptophan, showed no statistically significant differences between the different age groups. When comparing the mean differences in individual AA among these three age groups using the post-hoc test, alanine, tyrosine, phenylalanine, glycine, glutamine, cystine, homocystine, isoleucine, gamma-aminobutyric acid and tryptophan appeared to be constant across all age groups. Glutamic acid and serine correlated significantly with age (p<0.05), with a definite decline in concentration from infancy to adulthood (r=0.396 and 0.243; p<0.01, respectively). We conclude that AA values are not evidently affected by race, but they do vary with age.

Adolescent↗
PubMed1998

[Delayed effects of organochlorine pesticides in man].

Available information on organochlorines and the chronic effects of exposure to them are set out. Organochlorinated compounds are the most persistent pesticides and can be found in all ecosystems. Although they are generally efficient in pest control, they are also a potent environment pollutant and can provoke health problems in man. The evidences of the carcinogenic potential of organochlorines are controversial and insufficient, but they have been related to an increase in the incidence of some kinds of tumors, such as leukemia and solid tumors. Reproductive effects, due to anti-androgenic and estrogenic action, on embryonic virilization, the incidence of abortion and the frequency of prematurity, have also been observed. The accumulation of the organochlorines in the adipous tissue is positively correlated to the increase in aging and could be implicated in the development of aging diseases, such as Parkinson's disease. The effects of pesticides on human health have not yet been completely elucidated. Genotoxicity is one of the most serious of the possible harmful effects caused by these compounds and calls for special attention in view of the irreversible nature of the process and to the long latency associated with its manifestation.

Environmental Exposure↗
PubMed2005

Flow-through chloroquine sensor and its applications in pharmaceutical analysis.

Poly (vinyl chloride) membrane electrodes that responded selectively towards the antimalarial drug chloroquine are described. The electrodes were based on the use of the lipophilic potassium tetrakis(4-chlorophenyl)borate as ion-exchanger and bis(2-ethylhexyl)adipate (BEHA), or trioctylphosphate (TOP) or dioctylphenylphosphonate (DOPP) as plasticizing solvent mediator. All electrodes produced good quality characteristics such as Nernstian- and rapid responses, and are minimally interfered with by the alkali and alkaline earth metal ions tested. The membranes were next applied to a flow-through device, enabling it to function as flow-injection analysis (FIA) detector. The performance of the sensor after undergoing the FIA optimization was further evaluated for its selectivity characteristics and lifetime. Results for the determination of chloroquine in synthetic samples that contained common tablet excipients such as glucose, starch, and cellulose, and other foreign species such as cations, citric acid or lactic acid were generally satisfactory. The sensor was also successfully used for the determination of the active ingredients in mock tablets, synthetic fluids and biological fluids. The sensor was applied for the determination of active ingredients and the dissolution profile of commercial tablets was also established.

Antimalarials↗
PubMed1992

A net carbohydrate and protein system for evaluating cattle diets: II. Carbohydrate and protein availability.

The Cornell Net Carbohydrate and Protein System (CNCPS) has a submodel that predicts rates of feedstuff degradation in the rumen, the passage of undegraded feed to the lower gut, and the amount of ME and protein that is available to the animal. In the CNCPS, structural carbohydrate (SC) and nonstructural carbohydrate (NSC) are estimated from sequential NDF analyses of the feed. Data from the literature are used to predict fractional rates of SC and NSC degradation. Crude protein is partitioned into five fractions. Fraction A is NPN, which is trichloroacetic (TCA) acid-soluble N. Unavailable or protein bound to cell wall (Fraction C) is derived from acid detergent insoluble nitrogen (ADIP), and slowly degraded true protein (Fraction B3) is neutral detergent insoluble nitrogen (NDIP) minus Fraction C. Rapidly degraded true protein (Fraction B1) is TCA-precipitable protein from the buffer-soluble protein minus NPN. True protein with an intermediate degradation rate (Fraction B2) is the remaining N. Protein degradation rates are estimated by an in vitro procedure that uses Streptomyces griseus protease, and a curve-peeling technique is used to identify rates for each fraction. The amount of carbohydrate or N that is digested in the rumen is determined by the relative rates of degradation and passage. Ruminal passage rates are a function of DMI, particle size, bulk density, and the type of feed that is consumed (e.g., forage vs cereal grain).

Animal Feed↗
PubMed1976

Metabolism of linoleamides. I. Absorption, excretion and metabolism of N-(alpha-methylbenzyl)linoleamide in rat and man.

1. In urine of rats dosed with N-(alpha-methylbenzyl)linoleamide (MBLA), three dicarboxylic acid monoamides, N-(alpha-methylbenzyl)succinic acid monoamide, N-(alpha-methylbenzyl)glutaric acid monoamide and N-(alpha-methylbenzyl)adipic acid monoamide, were identified. Conjugated alpha-methylbenzylamine, hippuric acid and conjugates of the dicarboxylic acid monoamides were also found in the urine. N-(alpha-Methylbenzyl)succinic acid monoamide was the main metabolite in rats. 2. Biliary excretion of radioactivity was studied in rats, cannulated for collection of bile and duodenal infusion, after oral administration of N-(alpha-methylbenzyl)[1-14C]linoleamide. With constant duodenal infusion of bile, about 7% of the dose was excreted in the bile, while excretion of radioactivity was negligible without bile infusion. 3. The g.l.c. analysis of human urine after oral administration of MBLA revealed that two dicarboxylic acid monoamides were present and N-(alpha-methylbenzyl)succinic acid monoamide was the main metabolite. 4. MBLA was excreted unchanged in the faeces of men who received MBLA to the extent of about 53% dose in 3 days. 5. MBLA was not detected (less than 1 mug/ml) in the serum of a volunteer who had been taking an oral daily dose of 1500 mg of MBLA for 3 months.

Administration, Oral↗
PubMed1981

Guanidination of the lysine residues present in fibrous elastin and in soluble elastin peptides.

We have found that only 20 to 30% of the lysine residues measured after acid hydrolysis of insoluble elastin and alpha-elastin were blocked by prior guanidination of elastin with o-methylisourea. In contrast free lysine was guanidinated almost 100% and a purified, highly crosslinked peptide fraction of low molecular weight, 85%. The non-reactivity of lysine does not seem to be due to steric hindrance in the fibrous protein or in the large peptides derived therefrom but rather to the presence of epsilon [delta-adipic acid]-lysine, the oxidized form of lysinonorleucine described by Bailey et al. Since photolysis of desmosine and isodesmosine leads also to the formation of new lysine residues, methods will have to be devised to distinguish lysine-containing peptides derived from photolyzed elastin.

Amino Acids↗