Prenatal effects of DuP-697—the irreversible, highly selective cyclooxygenase-2 inhibitor

Burdan, Franciszek; Dudka, Jarosław; Szumiło, Justyna; Korobowicz, Agnieszka; Klepacz, Lidia

doi:10.1016/s0890-6238(03)00045-5

Cited by 21 publications

(18 citation statements)

References 41 publications

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“…19 and 20). This panel of COX inhibitors consisted of ASA, a relatively non-specific COX inhibitor, though with greater activity toward the COX-1 isoform, 21 DuP-697 (5-bromo-2-(4-fluorophenyl-3-(4-methylsufonyl) phenylthiophene), a predominantly COX-2 inhibitor, 22 FR 122047 (1-[[4,5-bis(4-methoxyphenyl)-2-thiazolyl]carbonyl]-4-methyl-piperazine, monohydrochloride hydrate), a selective COX-1 inhibitor 23 and INDO (1-(chlorobenzoyl)-5-methoxy-2-methyl-3-indoleacetic acid), 24 a rather non-specific inhibitor, though with greater activity against COX-1. For a positive control of enhancement of 1,25D-induced differentiation we used SB202190, an inhibitor of p38MAP kinase with a known ability to increase the JNK pathway activity in myeloid leukemia cells.…”

Section: Resultsmentioning

confidence: 99%

Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1, 25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling

Jamshidi

Zhang²,

Harrison³

et al. 2008

Cell Cycle

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Section: Resultsmentioning

confidence: 99%

Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1, 25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling

Jamshidi

Zhang²,

Harrison³

et al. 2008

Cell Cycle

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“…This mechanism also explains the good prenatal tolerance of COX-2 selective compounds, which induce only intrauterine growth retardation when administered at high doses. Retardation seems to be secondary to COX-2 inhibition in late pregnancy (16,24). On the other hand, single cases of VSDs and gastroschisis were observed in fetuses treated in utero with very high dose of CJ-19,209 (19) and DFU (16), respectively.…”

Section: Discussionmentioning

confidence: 99%

“…The primary mechanism underlying VSDs, MDs, diaphragmatic hernia (15)(16)(17), and skeletal anomalies (15,16,24) has been associated with prenatal COX-1 blockade and disturbances in eicosanoid physiology. COX-1 is the only COX isoenzyme which was detected throughout the whole embryonic and fetal period, and could regulate prostaglandins, prostacyclin and thromboxane synthesis (35).…”

Section: Discussionmentioning

confidence: 99%

“…Animals were obtained from a commercial breeder (Rembertow, Warsaw, Poland) and kept under standard laboratory conditions as previously described (24)(25)(26)(27). The initial body weight of the dams on insemination day (gestational day 1, GD 1), ranged from 200 to 250 g. Commercial laboratory rat chow (LSM ® ; Agropol, Motycz, Poland) and filtered municipal tap water (Lublin, Poland) were provided ad libitum.…”

Section: Methodsmentioning

confidence: 99%

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Congenital ventricular septal defects and prenatal exposure to cyclooxygenase inhibitors

Burdan

Szumiło

Dudka

et al. 2006

Braz J Med Biol Res

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Ventricular septal defects (VSDs) are common congenital abnormalities which have been reported to be associated with maternal fever and various environmental factors. The aim of the present study was to evaluate the effect of prenatal exposure to cyclooxygenase (COX) inhibitors on heart defects. A retrospective statistical analysis was performed using data collected in our laboratory during various teratological studies carried out on albino CRL:(WI)WUBR Wistar strain rats from 1997 to 2004. The observations were compared with concurrent and historic control data, as well as findings from other developmental toxicological studies with selective and nonselective COX-2 inhibitors. Despite the lack of significant differences in the frequency of VSDs between drug-exposed and control groups, statistical analysis by the two-sided Mantel-Haenszel test and historical control data showed a higher incidence of heart defects in offspring exposed to nonselective COX inhibitors (30.06/10,000). Unlike other specific inhibitors, aspirin (46.26/10,000) and ibuprofen (106.95/ 10,000) significantly increased the incidence of the VSD when compared with various control groups (5. 38-19.72/10,000). No significant differences in length or weight were detected between fetuses exposed to COX inhibitors and born with VSD and non-malformed offsprings. However, a statistically significant increase of fetal body length and decrease of body mass index were found in fetuses exposed to COX inhibitors when compared with untreated control. We conclude that prenatal exposure to COX inhibitors, especially aspirin and ibuprofen, increased the incidence of VSDs in rat offspring but was not related to fetal growth retardation.

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“…The authors described the dose-dependent intrauterine growth restriction of laboratory animal foetuses [5,7,8,10,22]. It is also important to note that in the case of COX-2 inhibitors, the described complication appeared after the administration of high doses, exceeding the threshold of selectivity [9,12].…”

Section: Current Issues In Pharmacy and Medical Sciencesmentioning

confidence: 99%

Organ and prenatal toxicity of nonsteroidal anti-inflammatory drugs

Dyndor

Dworzański

Pliszczynska-Steuden

et al. 2015

Current Issues in Pharmacy and Medical Sciences

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Non-selective cyclooxygenase (COX) inhibitors, commonly referred to as nonsteroidal anti-inflammatory drugs (NSAIDs), are among the most taken pharmaceuticals. In adults, they can have a series of side effects, including especially gastroenterotoxicity, hepatotoxicity, nephrotoxicity, chondrotoxicity, and neurotoxicity, and they can induce allergic reactions. Any exacerbation of symptoms depends on the chemical structure of the drug, its dosage and duration of exposure, individual sensitivity, comorbidities and the degree of inhibition of basic COX isoenzymes -the constitutive (COX-2) and induced (COX-1) expressions. However, data on prenatal toxicity are inconsistent. Classic nonselective COX inhibitors do not result in an increase in the risk of developing significant congenital defects; however, if used in the late-pregnancy period, they can have an adverse effect on the foetus, by inducing the premature closure of the ductus arteriosus and by producing a tocolytic effect. Individual reports also indicate the increased risk of developing heart and anterior abdominal wall defects, as well as hypospadias.

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Prenatal effects of DuP-697—the irreversible, highly selective cyclooxygenase-2 inhibitor

Cited by 21 publications

References 41 publications

Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1, 25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling

Induction of differentiation of human leukemia cells by combinations of COX inhibitors and 1, 25-dihydroxyvitamin D3 involves Raf1 but not Erk 1/2 signaling

Congenital ventricular septal defects and prenatal exposure to cyclooxygenase inhibitors

Organ and prenatal toxicity of nonsteroidal anti-inflammatory drugs

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