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Biomedical subjects

Franciszek Burdan

Publications and source records attributed to Franciszek Burdan.

At least 19 recordsLinked to original sources
PubMed2006

Celosomy is associated with prenatal exposure to cyclooxygenase inhibitors.

Celosomy is a term used for a group of congenital anomalies characterized by opening of the somatic wall with evisceration. The most common types of celosomy are gastroschisis and omphalocele. They have been associated with maternal age, cigarette smoking, environmental pollution, as well as prenatal exposure to vasoconstrictors and recreational drugs. The aim of this study was to evaluate the effect of prenatal exposure to various selective and non-selective cyclooxygenase-2 (COX-2) inhibitors on the abdominal wall defects in rat. A retrospective statistical analysis was performed on the basis of data collected in our laboratory in the years 1997-2004, during different teratological studies with COX-inhibitors (aspirin, DFU, DuP-697, ibuprofen, paracetamol, piroxicam, propyphenazone, tolmetin). Out of 6744 live born fetuses celosomy was revealed only in four animals exposed to different non-selective COX inhibitors. A single case of gastroschisis was also found in a rat exposed to the selective COX-2 inhibitor. The fetal body weight was significantly lower in COX-exposed group of fetuses when compared with untreated control. It was also significantly decreased in non-malformed fetuses prenatally exposed to COX inhibitors when compared with untreated control. The fetal body weight and length were lower in fetuses born with gastroschisis than with omphalocele. However, when animals with both anomalies were pooled in one group the mean fetal body weight was marginally lower (p = 0.0523) when compared with non-malformed group, while no statistically significant differences were found for fetal length. The pooled statistical analysis done for the concurrent and our own historic data showed that only aspirin statistically increased the risk of abdominal wall defects in rat fetuses. The expected ratio for aspirin is 56.41 per 10,000 offsprings (p < 0.05), which is over 10-times higher than ratio for all non-selective COX inhibitors, including aspirin (6.01/10,000; p < 0.05). No differences were found for selective COX-2 inhibitors. It could be stressed that aspirin, unlike other non-selective and selective COX-2 inhibitors increases the risk of the abdominal wall defects, which are observed more often in growth-retarded fetuses.

Abnormalities, Drug-Induced↗
PubMed2006

[Cyclooxygenase and prostanoids--biological implications].

Arachidonic acid is the main precursor of eikosanoids, which regulate the function of various organs and systems. It is released from cellular membrane phospholipids by phospholipase A2 or indirectly by phospholipases C and D. Prostaglandins, prostacyclin (PGI2), and thromboxane A2 (TAX2) are synthesized from arachidonic acid on a metabolic pathway dependent on prostaglandin H2 synthase activity, also known as cyclooxygenase (COX). Of the 12 prostaglandins, the most potent are PGD2, PGE2, and PGF2. The others are synthesized in a primary step of arachidonic acid transformation (PGG2, PGH2), by degradation of the above-mentioned prostaglandins, or are not presented physiologically and may be chemically generated (PGK2, PGL2). Similar compounds could originate from dihomo-gamma-linolenic, alpha-linoleic, and eicosapentaenoic acids. Three primary COX isoenzymes are distinguished: COX-1 (constitutive), COX-2 (inducible), and COX-3, which is detected mainly in the central nervous system. A number of partial forms of COX-1 and COX-2 are also known, but their biological functions have not been well evaluated. Although they differ in genes, transcription factors, primary protein structure, reactivity to substrates, and drugs which inhibit enzyme activity, the crystal structure is similar for all the izoenzymes. In contrast to the COX-1 gene, whose expression is typical for most of the cells, constant COX-2 expression was detected in the placenta and fetal tissue in late pregnancy. In the postnatal period, COX-2 expression decreases rapidly physiologically, and is observed in kidney, forebrain, spinal cord, as well as some other organs, but to a minor degree. It increases in inflammatory, degenerative, and neoplastic processes.

Animals↗
PubMed2006

[Wilson's principles--a base of modern teratology].

Wilson's principles were formulated after thalidomide tragedy. They become a fundamental for teratological studies with drugs and other factors that may disturb fetal development. It is postulated that susceptibility to teratogen depends on the genotype and developmental stage of the conceptus. Teratogenic agents act in specific manner on developing cells and tissues. The exposition depends on the agent's nature and availability. Manifestations of deviant development depends on the dosage and exposure frequency. In case of abnormal development the final manifestations include death of embryo or fetus, malformation, growth retardation and functional disorder.

Abnormalities, Drug-Induced↗
PubMed2005

Skeletal developmental effects of selective and nonselective cyclooxygenase-2 inhibitors administered through organogenesis and fetogenesis in Wistar CRL:(WI)WUBR rats.

Cyclooxygenase (COX) inhibitors are the most commonly ingested drugs. The aim of the study was to evaluate the prenatal skeletal effect of selective (DFU) and nonselective (tolmetin, ibuprofen, piroxicam) COX-2 inhibitors. All the tested compounds were administered intragastrically to pregnant Wistar rats from 7 to 21 gestation day. The initial dose was set at 8.5mg/kg/dose for tolmetin and ibuprofen, 0.3 and 0.2mg/kg/dose for piroxicam and DFU. The middle dose was increased 10-times. The highest dose, except for ibuprofen, was elevated 100-times. The highest dose for ibuprofen was set at 200mg/kg/dose. Tolmetin and ibuprofen were administered three times a day. Piroxicam and DFU were dosed once daily. After routine teratological examinations, extremities of randomly selected 21-day-old fetuses were taken for histological, immunohistochemical and molecular studies. The proximal femoral epiphyses were separated and their ultrastructure evaluated. The expression of genes coding cytokines (IL-1alpha, IL-1beta, IL-6, TNF-alpha, TNF-beta) and proteins (COX-1, COX-2, cathepsin K, collagen types I, II and X; osteocalcin, osteopontin) was evaluated in femoral epiphyses by RNase Protection Assay and/or immunohistochemically. The articulate development was checked histologically and found undisturbed in any of the experimental groups. The epiphysis of the 21-day-old fetuses, presented physiological expression of COX-1 and COX-2, as well as cathepsin K, collagen types I, II and X; osteopontin, osteocalcin and TNF-alpha. Increased developmental skeletal variation was noted in groups exposed to the highest dose of nonselective drugs. Unlike the increased number of skeletal variations observed in fetuses exposed to highest doses of nonselective compounds, both groups of COX inhibitors did not disturb joint formation and morphology of femoral epiphyses when administered even in high maternal toxic doses.

Animals↗
PubMed2005

Comparison of developmental toxicity of selective and non-selective cyclooxygenase-2 inhibitors in CRL:(WI)WUBR Wistar rats--DFU and piroxicam study.

BACKGROUND: Cyclooxygenase (COX) inhibitors are one of the most often ingested drugs during pregnancy. Unlike general toxicity data, their prenatal toxic effects were not extensively studied before. The aim of the experiment was to evaluate the developmental toxicity of the non-selective (piroxicam) and selective (DFU; 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl) phenyl-2(5H)-furanon) COX-2 inhibitors. METHODS: Drugs were separately, orally once daily dosed to pregnant rats from day 8 to 21 (GD1=plug day). Doses were set at 0.3, 3.0 and 30.0mg/kg for piroxicam and 0.2, 2.0 and 20.0mg/kg for DFU. Fetuses were delivered on GD 21 and routinely examined. Comprehensive clinical and developmental measurements were done. The pooled statistical analysis for ventricular septal (VSD) and midline (MD) defects was performed for rat fetuses exposed to piroxicam, selective and non-selective COX-2 inhibitor based on present and historic data. RESULTS: Maternal toxicity, intrauterine growth retardation, and increase of external and skeletal variations were found in rats treated with the highest dose of piroxicam. Decrease of fetal length was the only signs of the DFU developmental toxicity observed in pups exposed to the highest compound dose. Lack of teratogenicity was found in piroxicam and DFU-exposed groups. Prenatal exposure to non-selective COX inhibitors increases the risk of VSD and MD when compared to historic control but not with selective COX-2 inhibitors. CONCLUSION: Both selective and non-selective COX-2 inhibitors were toxic for rats fetuses when administered in the highest dose. Unlike DFU, piroxicam was also highly toxic to the dams. Prenatal exposure to selective COX-2 inhibitors does not increase the risk of ventricular septal and midline defects in rat when compared to non-selective drugs and historic control.

Abdominal Wall↗
PubMed2005

Activity of NADPH-cytochrome P-450 reductase of the human heart, liver and lungs in the presence of (-)-epigallocatechin gallate, quercetin and resveratrol: an in vitro study.

NADPH-cytochrome P-450 reductase (P-450 reductase) plays a crucial role in the metabolism of many endogenic compounds and xenobiotics detoxication. The enzyme is also involved in the toxicity of some clinically important antitumour drugs (doxorubicin) and pesticides (paraquat). P-450 reductase activates them to their more toxic metabolites via one electron reduction which triggers free radical cascade. In some cases however, such transformation is essential to produce therapeutic effect in anticancer drugs. The main purpose of the paper was to evaluate the effect of three natural compounds found in human diet: (-)-epigallocatechin gallate (EGCG), quercetin and resveratrol on P-450 reductase activity. The activity of the enzyme was determined spectrophotometrically by measurement of the rate of cytochrome c reduction at 550 nm, in vitro, using human heart, liver and lung microsomes. It was found that quercetin increased the P-450 reductase activity in human organs at all tested doses. The activity of microcosms in all organs was enhanced according to the concentrations of quercetin, which increased the activity in the order lung>heart>liver. Addition of EGCG to the reaction mixture enhanced the P-450 reductase activity in the following order: liver>heart>lung. However, no significant effect of resveratrol on P-450 reductase activity was observed. It seems that the presence of quercetin and EGCG in the diet may increase P-450 reductase activity during doxorubicin therapy with subsequent increased risk of toxicity. A beneficial effect may be obtained in anticancer therapy with bioreductive agents like tirapazamine.

Anti-Bacterial Agents↗
PubMed2005

Morphological studies in modern teratological investigations.

Despite the variety of modern molecular techniques available, examination of foetal anatomy is still a fundamental part of teratological studies in evaluating the developmental toxicity of xenobiotics or other non-chemical factors. The article presents contemporary methods of embryotoxicity and foetotoxicity assessment. A single alizarin red S and double alcian blue followed by alizarin red S staining, as well as various methods of soft tissue examination are discussed.

Alcian Blue↗
PubMed2005

[The effect of cyclooxygenase inhibitors on the bone and cartilage].

The experimental studies showed that cyclooxygenase inhibitors, decrease bone demineralization, prolong fracture healing and assimilation of bone grafts and implants. Due to chemical structure drugs inhibit, stimulate or do not significantly change cartilage matrix synthesis. In case of in-utero exposure non-selective drugs may induce skeletal developmental variations, which depends on the used dose and COX-1 inhibition potency.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2005

[Development and congenital malformations of the skeleton].

The article presents current knowledge on skeleton development, which is initiated by mesenchymal cells condensation. The mesenchymal to epithelial transformation, vascular regression, cartilage formation and ossification are involved in normal skeletogenesis. All the processes are influenced by various genes and regulatory molecules, e.g., N-cadherin, vascular endothelial growth factor, transforming growth factor-beta, syndecan-3 and others. The chondrogenesis depends on the Sox genes expression - Sox5, Sox6 and especially Sox9, which continued action produce persistent cartilage. The essential role in osteogenesis is played by the transcription factor Runx2 that directly activates expression of genes coding typical bone proteins like collagen type I, osteocalcin, osteopontin and osteonectin. Development of fibrous, cartilaginous and synovial joints, bone maturation and remodeling, and mechanisms leading to skeleton dysmorphogenesis are also discussed.

Antigens, CD↗
PubMed2004

Developmental toxicity evaluation of ibuprofen and tolmetin administered in triple daily doses to Wistar CRL:(WI)WUBR rats.

BACKGROUND: Ibuprofen and tolmetin are popular non-steroidal anti-inflammatory drugs. Previous animal studies taken with single daily doses showed their good prenatal tolerability. However, since both cyclooxygenase (COX) inhibitors have a short half-life, the current report presents drug developmental effects after triple daily doses administration, as they are used in human. METHODS: Drugs were separately, orally dosed to pregnant rats triple daily 8 hr apart from day 8 to 21 (GD=1-plug day). The total daily doses were set at 25.5, 255.0, and 600.0 mg/kg for ibuprofen and 25.5, 255.0, and 2550.0 mg/kg for tolmetin. Fetuses were delivered on GD 21 and routinely examined. Comprehensive clinical and developmental measurements were done. RESULTS: Maternal toxicity and intrauterine growth retardation were found in groups exposed to the highest doses of both drugs. An increase of external variations was reported in groups exposed to the middle and highest dose of ibuprofen and to the highest dose of tolmetin. Skeletal variations were significantly different only in litters treated with the highest doses of the drugs. Pooled statistical analysis showed a higher incidence of midline and ventricular septal (VSD) defect in rat fetuses exposed to COX inhibitors when compared with historical control data. For ibuprofen, the influence on VSD was similar to aspirin. CONCLUSION: Both COX inhibitors were toxic to dams in the highest doses evaluated, which caused a significantly greater incidence of intrauterine growth retardation and developmental variations.

Animals↗
PubMed2004

Gastrointestinal and hepatic toxicity of selective and non-selective cyclooxygenase-2 inhibitors in pregnant and non-pregnant rats.

The aim of the study was to evaluate the toxicity of non-selective (tolmetin, ibuprofen and piroxicam) and selective (DFU) cyclooxygenase-2 inhibitors on pregnant and non-pregnant rats. The drugs were administered orally once (DFU, piroxicam) or three times (tolmetin, ibuprofen) a day from days 8 through 21 of gestation experiment in three doses. The initial dose was similar to the human antiinflammatory one and set as 8.5 mg/kg (tolmetin, ibuprofen), 0.3 mg/kg (piroxicam) and 0.2 mg/kg (DFU). The middle dose was increased 10 times and the highest one 100 times the initial dose. The highest dose for ibuprofen was set at 200mg/kg due to high mortality. On gestation/experimental day 21 animals were sacrificed, blood was collected and abdominal organs were taken for pathological examination. Activity of alanine and asparate aminotransferases and levels of total protein and urea were determined. Stomach, small and large intestines, and liver were grossly and histologically examined. Dose-dependent mortality, signs of gastrointestinal toxicity, and significant changes of biochemical parameters were found in groups exposed to non-selective COX inhibitors in both pregnant and non-pregnant rats. Mild regressive structural hepatic changes were observed. Significant decrease of protein level in non-pregnant rats treated with high DFU dose, and occasionally observed gastrointestinal changes were the only changes noted in groups exposed to the selective COX-2 inhibitor. Tolerability of non-selective COX inhibitors was lower in both pregnant and non-pregnant groups when compared with DFU. Insignificant mortality and histological changes were noted between pregnant and non-pregnant groups.

Animals↗
PubMed2004

Human skeletal muscle lactate dehydrogenase activity in the presence of some alcohol dehydrogenase inhibitors.

Methanol, ethylene glycol and other alcohol intoxications are complicated by severe acidosis which could be caused by formation of metabolic acids and additionally lactic acid production. An increasing nicotinamide adenine dinucleotide reduced/nicotinamide adenine dinucleotide oxidized (NADH/NAD) ratio during alcohol biotransformation is responsible for the induction of lactic acidosis. The main purpose of the present paper was to evaluate the effect of 4-methylpyrazole, cimetidine, ethylenediaminetetraacetic acid disodium salt, ethanol and methanol on lactate dehydrogenase (E.C. 1.1.1.27) activity and to discuss this issue. The activity of the enzyme was determined spectrophotometrically, in vitro using human enzyme skeletal muscle homogenates. 4-Methylpyrazole, cimetidine and ethylenediaminetetraacetic acid disodium salt at concentrations 0.01, 0.1, 1.0 mM and 12.5, 25.0, 50.0 mM of ethanol and methanol were studied. Our results showed that cimetidine increased lactate dehydrogenase activity as compared to the control at all tested concentrations. Such activity was noted for 4-methylpyrazole at 0.1 mM and higher concentration. By contrast, no significant effect on lactate dehydrogenase activity in the presence of ethylenediaminetetraacetic acid disodium salt, methanol and ethanol was observed.

Alcohol Dehydrogenase↗
PubMed2004

[Human erythrocyte lactate dehydrogenase activity changes in the presence of some alcohol dehydrogenase inhibitors].

The aim of the study was to evaluate the effect of alcohol dehydrogenase (ADH; E.C. 1.1.1.1) inhibitors and substrates: cimetidine, 4-methylpyrazole (4MP), EDTA, ethanol and methanol on lactate dehydrogenase (LDH; E.C. 1.1.1.27) activity. The activity of LDH was spectrophotometrically determined in in-vitro prepared diluted hemolysates obtained from human erythrocytes with mentioned compounds at the concentrations 0.01, 0.1, 1.0 mM of cimetidine, EDTA, 4MP and 12.5, 25.0, 50.0 mM of ethanol and methanol. The reaction was conducted at 37 degrees C in pH 7.5 and changes of optical density was measured at lambda = 340nm. LDH activity was significantly inhibited by 0.10 mM (p < 0.05) and 1.0 mM (p < 0.01) of cimetidine and EDTA. There were no observed any significant changes vs. control in LDH activity when 4MP, ethanol or methanol was added to environment of reaction.

Adult↗
PubMed2004

Variation in morphology of the valve of the great cardiac vein in the human hearts.

The research was carried on 70 hearts of adult humans. The hearts were subjected to direct analyses on the autopsy material. The presence or absence of the valve of the great cardiac vein was analysed with reference to sex. The terminal valve of the great cardiac vein was found in 92% of the examined hearts. To define the location of the valve of the great cardiac vein the osmium of the left atrium oblique vein was treated as the reference point. In 3% of cases the presence of the valve was observed independently of the opening of the left atrium oblique vein. The valve of the great cardiac vein was placed proximally from the opening of the left atrium oblique vein. The valve of the great cardiac vein placed distally in relation to the beginning of the coronary sinus was never observed. The three types of the great cardiac vein valves were found: 1. single, semilunar cusp; 2. endothelial fold; 3. double pouches.

Adolescent↗
PubMed2003

Morphology of third molar teeth with incompletely formed apices on the basis of panoramic radiograms.

Third molar teeth are causative factors of many oral pathologies. Lower third molars are the most often retained teeth and the origin of considerable pain. The aim of the study is a presentation of the morphology of third molars with incompletely formed apices on the basis of panoramic radiograms. The material comprised routine panoramic radiograms taken in the years 1996-2000. In the cases where third molars with incompletely formed apices were found, there was determined the location of the teeth in the alveolar process. The angle between occlusal plane and tooth axis was measured, which allowed determination of angularity of the teeth. Retromolar space width ratio was also calculated as a prognostic radiographic feature on which an estimation of future eruption of mandibular third molars could be based. In retained teeth the reasons for impaction, such as incorrect angularity, insufficient retromolar space, presence of pathological lesions impeding eruption, were analysed. Panoramic radiograms proved useful in diagnostics of morphology of third molars with incompletely formed apices.

Adolescent↗
PubMed2003

[Coxibs: highly selective cyclooxygenase-2 inhibitors. Part I. Clinical efficacy].

Slow, time-dependent, irreversible, highly selective inhibitors of COX-2 (coxibs) have been used for the treatment of osteoarthritis and rheumatoid arthritis, as well as other disease entities such as acute pain, fever, neoplastic changes, and Alzheimer's disease, the pathomechanism of which is dependent on the coexisting inflammatory process or overexpression of cyclo-oxygenase (COX) genes. The article presents current state of knowledge about the clinical efficacy of coxibs (celecoxib, rofecoxib) compared to non-selective COX inhibitors. The physiology and pathophysiology of both COX isoforms (COX-1, COX-2) are also discussed.

Alzheimer Disease↗