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At least 649 records · Page 36Linked to original sources
PubMed1985

Can collagen metabolism be controlled: theoretical considerations.

Pharmacologic alterations of the inflammatory response and collagen metabolism will lead to control of the many disease states of fibrosis. Many of these diseases kill and cripple far more than hypertrophic scar. Far too little research is being directed in this area. The objectives of controlling fibrosis by interfering with collagen crosslinking were defined clearly by Peacock. Perhaps topical BAPN will be the first agent to bring a practical clinical reality to his predictions made over 20 years ago.

Aminopropionitrile↗
PubMed1983

Mononuclear cell factors that inhibit fibroblast collagen synthesis. I. In vitro conditions determining their production and expression.

Peripheral blood mononuclear cells (PBMC) incubated either with phytohaemagglutinin-P (PHA) under serum-free conditions or with tuberculin purified protein derivative in the presence of 5% human blood group AB serum released into the culture medium factors that decreased collagen synthesis by dermal fibroblasts. These factors were first detected after incubation of PBMC with PHA for 24 h and were produced by non-adherent cells. The decrease in collagen synthesis was observed despite changes in conditions of fibroblast culture, the addition of a cross-linking inhibitor, and the use of different fibroblast cell lines.

Aminopropionitrile↗
PubMed1982

Wound healing: a review. IV. Systemic medications affecting wound healing.

Physicians performing dermatologic surgery should include a thorough drug history in their preoperative assessments of patients. Such information may allow for the discontinuation, if desired, of drugs that negatively influence the wound-healing process. In some instances, the surgeon may find it useful, during the perioperative period, to substitute a drug known to impede wound healing with another possessing no untoward effects. In other situations, as in the treatment of keloids, physicians may wish to introduce drugs known to reduce scar formation into the biologic environment in which wound healing ensues.

Adrenal Cortex Hormones↗
PubMed1979

Possible modification of scar tissue by biochemical methods.

This paper reviews some of the biochemical modifications involved in fibrous tissue formation and discusses possible ways of controlling fibrosis in clinical conditions. The lathyritic agents, beta-aminoproprionitrile (BAPN) and penicillamine, appear in certain situations to be able to control fibrosis by blocking the biosynthesis of collagen. There are no compounds that are yet known which are capable of reversing pre-existing fibrosis and future research may perhaps be more profitably directed towards the stimulation of collagen catabolism rather than the inhibition of its synthesis.

Aminopropionitrile↗
PubMed1990

Further studies on the metabolism of methylamine by semicarbazide-sensitive amine oxidase activities in human plasma, umbilical artery and rat aorta.

An ion exchange radiochemical assay has been developed to study the deamination of [14C]methylamine (MA) in homogenates of rat aorta and human umbilical artery, as well as in samples of human plasma. MA metabolism was found to be inhibited almost completely by 1 mM semicarbazide, but virtually unaffected by 0.1 mM clorgyline, suggesting that MA is a substrate for the semicarbazide-sensitive amino oxidase (SSAO) activities which also metabolize benzylamine (BZ) in these sources. Mean Km values for MA metabolism by aorta, umbilical artery and plasma were 182, 832 and 516 microM, respectively, with corresponding Vmax values in aorta and umbilical artery of 100 and 590 nmol (mg prot.)-1 h-1, and in plasma of 48 nmol (mL serum)-1 h-1. Kinetic constants determined for [14C]BZ metabolism in plasma (by an organic solvent extraction assay) and in umbilical artery (by the ion exchange assay) yielded mean Km values of 225 microM (plasma), 222 microM (umbilical artery), and Vmax values of 28 nmol (mL serum)-1 h-1 (plasma) and 377 nmol (mg prot.)-1 h-1 (umbilical artery). The deamination of [14C]MA was inhibited competitively by unlabelled BZ, with Ki values in umbilical artery and plasma of 220 and 172 microM, respectively. Also, metabolite formation from mixtures of [14C]BZ (200 microM) and [14C]MA (800 microM) was extremely close to that predicted for a single enzyme capable of metabolizing two alternative substrates in a competitive fashion.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopropionitrile↗
PubMed1985

The effect of a lathyritic diet on the sensitivity of tendon to strain rate.

While the tensile failure properties of rat-tail tendon depend on strain rate, the sensitivity to strain rate decreases with age, especially during sexual maturation. The object of this study was to determine the effect of an experimental model of chronic lathyrism on age-dependent changes in the sensitivity of developing tendon strength to strain rate. Tensile failure experiments were conducted at high and low strain rate on tendons excised from test and control animals aged 1 to 6 mo. The tensile "yield" response of tendon was significantly affected by the diet resulting in a reduced tensile strength and failure strain. While the sensitivity of tendon failure to strain rate was slightly elevated by the experimental diet, age-dependent changes compared with controls. Since the diet supplement is thought to inhibit covalent crosslinking of collagen in the developing tendon, other factors are likely responsible for decrease in the sensitivity of tendon strength to strain rate during maturation.

Aging↗
PubMed1982

Lung fibrosis and emphysema: divergent responses to a common injury?

Cadmium chloride, administered intratracheally to golden Syrian hamsters, causes an acute lung injury which evolves into a lesion with functional and morphological features of diffuse fibrosis. With simultaneous feeding of a lathyrogen, beta-aminoproprionitrile, this same injury evolves into functional and morphological changes of bullous emphysema. These results suggest that the same lung injury might result in either fibrosis or emphysema, connective tissue synthesis during the healing phase being the critical determinant.

Aminopropionitrile↗
PubMed2003

TGF-beta1 causes airway fibrosis and increased collagen I and III mRNA in mice.

BACKGROUND: Subepithelial collagen and extracellular matrix protein deposition are important pathophysiological components of airway remodelling in chronic asthma. Animal models based on the local reaction to antigens show structural alterations in the airway submucosal region and provide important information regarding disease pathophysiology. We describe a murine model of peribronchial fibrosis using intratracheally instilled transforming growth factor (TGF)-beta(1) in BALB/C mice that facilitates a mechanistic approach to understanding the cellular and molecular pathways leading to airway fibrosis. METHODS: BALB/C mice were intratracheally instilled with either TGF-beta(1) or buffered saline. Airway fibrosis was assessed by light microscopy, hydroxyproline content, and polymerase chain reaction (PCR) for collagen I and III on microdissected airway samples. The lysyl oxidase inhibitor beta-aminoproprionitrile (BAPN) was administered to TGF-beta(1) treated mice to block airway collagen deposition. Airway hyperresponsiveness was also measured after treatment with TGF-beta(1). RESULTS: During the 7 days after administration of TGF-beta(1) the mice developed increased subepithelial collagen which could be blocked by BAPN. Increased mRNAs for collagen types I and III were seen in microdissected airways 1 week after TGF-beta(1), and significantly increased total collagen was found in the airways 4 weeks after TGF-beta(1). A detectable increase in airway hyperreactivity occurred. CONCLUSIONS: This new model should facilitate detailed study of airway remodelling that occurs in the absence of detectable cellular inflammation, and allow examination of the functional consequences of a major structural alteration in the conducting airways uncomplicated by inflammatory cell influx.

Aminopropionitrile↗