The cardiotoxic effects of selective cyclo-oxygenase-2 inhibitors are well documented. Recently, concerns have been raised over the cardiovascular safety of nonselective nonsteroidal antiinflammatory drugs. The aim of this study was to assess the cardiac effects of diclofenac sodium on doxorubicin-induced cardiomyopathy in rats. Male Wistar rats were treated with doxorubicin (15 mg/kg intraperitoneally, single dose), diclofenac sodium (2.5 and 10 mg/kg/day, respectively, by gavage for 5 days) alone and doxorubicin + diclofenac sodium treatment, 24 hours after doxorubicin administration. Doxorubicin-induced a significant (P < 0.001) increase in the serum lactate dehydrogenase, cardiac thiobarbituric acid-reactive substance and catalase levels and a significant (P < 0.001) decrease in the cardiac glutathione and superoxide dismutase levels, which were significantly (P < 0.001) aggravated by diclofenac sodium treatment. Diclofenac sodium alone also showed a significant change in these parameters compared with the control. Ultrastructural studies showed that doxorubicin causes apoptosis in myocardium, which was characterized by condensation of chromatin network at the margins of nuclear membrane. Apoptosis induced by doxorubicin was exacerbated by diclofenac sodium treatment. Thus, our study indicates that diclofenac sodium, a nonaspirin nonsteroidal anti-inflammatory drug, is not free from cardiotoxicity and aggravates doxorubicin-induced cardiomyopathy in rats.
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http://dx.doi.org/10.1097/FJC.0b013e3181c87e17 | DOI Listing |
Environ Sci Pollut Res Int
January 2025
Department of Zoology, College of Science, King Saud University, P.O. Box 2455, 11451, Riyadh, Saudi Arabia.
Toxicol In Vitro
January 2025
Department of Basic Science, School of Medicine, Abadan University of Medical Sciences, Abadan, Iran.
The presence of pharmaceuticals in aquatic ecosystems and their impact on humans and the environment are growing concerns in environmental health. This study aimed to evaluate the potential reproductive effects of diclofenac, ibuprofen, and aspirin on dissociated ovarian and testicular cells from Arabian Sea bream, Acanthopagrus arabicus. The cells were exposed to varying concentrations of the pharmaceuticals for 48 h.
View Article and Find Full Text PDFSci Total Environ
January 2025
Uppsala Water and Waste Ltd, Box 1444, 751 44 Uppsala, Sweden.
Pharmaceuticals and per- and polyfluoroalkyl substances (PFAS) are persistent organic micropollutants (OMPs) posing environmental and health risks due to their bioaccumulative nature and potential toxicity. These OMPs spread to the environment due to the extensive use in today's society. Conventional wastewater treatment plants (WWTPs) are not designed to effectively remove these contaminants, making WWTPs an important pathway, especially for pharmaceuticals, to the aquatic environment.
View Article and Find Full Text PDFComput Biol Med
January 2025
National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India. Electronic address:
The biotransformation of drugs by enzymes from the human microbiome can produce active or inactive products, impacting the bioactivity and function of these drugs inside the human host. However, understanding the biotransformation reactions of drug molecules catalyzed by bacterial enzymes in human microbiota is still limited. Hence, to characterize drug utilization capabilities across all the microbial phyla inside the human gut, we have used a knowledge-based approach to develop HgutMgene-Miner software which predicts xenobiotic metabolizing enzymes (XMEs) through genome mining.
View Article and Find Full Text PDFPharmaceutics
January 2025
Department of Physics, Chemistry and Pharmacy, University of Southern Denmark, Campusvej 55, DK-5230 Odense, Denmark.
: The proton-coupled amino acid transporter (PAT1) is an intestinal absorptive solute carrier responsible for the oral bioavailability of some GABA-mimetic drug substances such as vigabatrin and gaboxadol. In the present work, we investigate if non-steroidal anti-inflammatory drug substances (NSAIDs) interact with substrate transport via human (h)PAT1. : The transport of substrates via hPAT1 was investigated in Caco-2 cells using radiolabeled substrate uptake and in oocytes injected with , measuring induced currents using the two-electrode voltage clamp technique.
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