This review describes cyclooxygenase (COX), which synthesizes prostanoids that play an important role in living things. The authors conducted a national and international literature review on the subject. The COX enzyme uses arachidonic acid to form prostanoids, which play a role in several physiological and pathological conditions. This enzyme has different isoforms, mainly COX-1 and COX-2. The constitutive isoform is COX-1, while COX-2 is the inducible isoform. Both are expressed in different tissues and at different levels, but they may also coexist within the same tissue. Both isoforms show essentially the same mode of action, but their substrates and inhibitors may differ. The COX-1 isoform, which plays a role in the continuation of physiological events, has an increased expression level in various carcinomas, and the COX-2 isoform, which is increased in inflammatory conditions, is typically expressed at low physiological levels in some tissues such as the brain, kidney, and uterus. In addition to investigating the efficacies of the COX-1 and COX-2 isoforms, the discovery of potential new COX enzymes and their effect continues. This review also looks at the roles of the COX enzyme in certain physiological and pathological conditions.

The aim of the present study was to determine the effects of florfenicol on the expected changes in sTNF-α, damage markers of the liver and kidney, and the lipid metabolism parameters in endotoxemic brown trout. Ninety-six brown trout were included in this study. After six of the fish were reserved as the control group, the remaining 90 fish were divided equally into 3 groups as follows: LPS (2 mg/kg, IP), LPS (2 mg/kg, IP) + florfenicol (40 mg/kg, IM), and florfenicol (40 mg/kg, IM). Blood samples were obtained from the tail of the fish at 1.5, 3, 6, 10, and 24 hours. The levels of sTNF-αwere determined by ELISA and biochemical markers were evaluated with an autoanalyzer. A significant increase was observed in the values of sTNF-αin the LPS and LPS + florfenicol groups (P<0.05). Significant increases were found in the kidney and liver damage determinants in the LPS and LPS + florfenicol groups (P<0.05). Irregular changes in the lipid metabolism parameters were observed in all the subgroups. In conclusion, florfenicol does not affect the increases of sTNF-αcaused by LPS and does not prevent liver or kidney damage; at least, it can be said that florfenicol does not have any evident positive effects on the acute endotoxemia of fish.

The aim of this study was to determine the anti-inflammatory effects of macrolides through kinetic parameters in bronchoalveolar lavage fluid (BALF) of lipopolysaccharide-induced lung injury. Rats were divided into four groups: lipopolysaccharide (LPS), LPS + tylosin, LPS + tilmicosin and LPS + tulathromycin. BALF samples were collected at sampling times. TNF, IL-1β, IL-6, IL-10 and 13,14-dihydro-15-keto-prostaglandin F₂α (PGM) and C-reactive protein (CRP) were analysed. Area under the curve (AUC) and maximum plasma concentration (C_max) values of inflammatory mediators were determined by a pharmacokinetic computer programme. When inflammatory mediator concentrations were compared between the LPS group and other groups for each sampling time, the three macrolides had no pronounced depressor effect on cytokine levels, but they depressed PGM and CRP levels. In addition, tylosin and tilmicosin decreased the AUC_0-24level of TNF, while tilmicosin decreased the AUC_0-24level of IL-10. Tylosin and tulathromycin decreased the AUC_0-24of PGM, and all three macrolides decreased the AUC_0-24of CRP. Especially tylosin and tulathromycin may have more expressed anti-inflammatory effects than tilmicosin, via depressing the production of inflammatory mediators in the lung. The AUC may be used for determining the effects of drugs on inflammation. In this study, the antiinflammatory effects of these antibiotics were evaluated with kinetic parameters as a new and different approach.

Nonsteroidal anti‐inflammatory drugs are frequently prescribed drug group in human and veterinary medicine. However, diclofenac, a traditional nonsteroidal anti‐inflammatory drug, related to cardiotoxicity is reported, and blood cardiac damage markers may increase within the first hours after damage. The aim of the current research was to determine the effect of diclofenac on the blood cardiac damage markers. Single dose of diclofenac (2.5 mg/kg, IM) was injected to 6 rams. Blood samples were collected in before (0 hour, control) and 6 hours after injection. Specific (troponin I, and creatine kinase‐MB) and nonspecific (lactate dehydrogenase, aspartate aminotransferase) blood cardiac damage marker concentrations, routine biochemical (hepatic damage, renal damage, lipid metabolism, glucose, and phosphorus) parameters, and hemogram values were measured. Diclofenac increased (P < 0.05) specific (troponin I) and nonspecific cardiac (lactate dehydrogenase, aspartate aminotransferase), hepatic (aspartate aminotransferase, alkaline phosphatase, and alanine aminotransferase), and muscular (creatine kinase) damage markers and high density lipoprotein level, while it decreased (P < 0.05) low density lipoprotein level. Moreover, diclofenac decreased (P < 0.05) white blood cell counts and increased (P < 0.05) red blood cell counts. In conclusion, it may be stated that diclofenac shows slight cardiotoxicity, whereas it may show potent hepatic and muscular damage effects at an intramuscularly single dose in sheep. Thereby, repeated injections of diclofenac may be more harmful in sheep.

Aim: It has been hypothesized that chondrotoxicity, the main side effect of enrofloxacin use, may be derived from oxidative stress, and this side effect can be confirmed by measuring malondialdehyde and endogen antioxidants following drug application. The primary aim of this research is to determine the effect of enrofloxacin on the joint fluid and blood oxidative status parameters, and it is also to determine the effect on the organ damage parameters. Materials and Methods: In the study, 10 rams received enrofloxacin (10 mg/kg/day, SC) for 14 days. Blood and joint fluids were taken on day 0 (Control) before drug application and 1.5 hours after the last drug application. Plasma and joint fluid malondialdehyde, total antioxidant status, superoxide dismutase, glutathione peroxidase and catalase levels were determined by an ELISA reader. Cardiac (CK-MB mass, troponin I), liver (AST, ALT, ALP, GGT, total protein, albumin) and kidney (Creatinine, BUN) damage markers and hemogram (WBC, RBC, platelet, hematocrit, haemoglobin) values were measured. Results: Enrofloxacin decreased the joint fluid catalase level (P<0.05), while there was no effect observed in the other oxidative status parameters of joint fluid or blood samples. Statistically significant changes (P<0.05) were found in some hemogram and biochemical parameters within the reference range. However, enrofloxacin increased (P<0.05) the levels of cardiac damage markers (CK-MB mass, troponin I). Conclusion: It may be stated that enrofloxacin does not cause oxidative stress in the joint fluid and blood in rams, and it is generally accepted to be safe when the effect on the organ/system is considered, but the long-term use and high doses require caution in terms of possible heart related damage.

The aim of this study was to determine the effect of azithromycin on LPS-induced pregnancy loss. Thirty-six pregnant female Wistar rats were divided into 4 equal groups as follows: control group, where 0.3mL of normal saline solution was administered intravenously on day 10 of pregnancy; azithromycin group, where azithromycin was administered orally at 350mgkg1 day on days 9, 10, and 11 of pregnancy; lipopolysaccharide group, where LPS was administered intravenously via the tail vein at 160μgkg1 on day 10 of pregnancy; and the azithromycin