Biochemical alterations in diclofenac-treated rats: Effect of selenium on oxidative stress, inflammation, and hematological changes

Abstract

We investigated the effect of selenium (Sel), a trace element in diclofenac sodium (DCF), nonsteroidal anti-inflammatory drugs-induced hepatic and renal toxicities in adult rats. Five experimental groups namely control, DCF (10 mg/kg), Sel (0.125 mg/kg), DCF + Sel (0.125 mg/kg), and DCF + Sel (0.25 mg/kg) consisting of 10 rats each were orally treated for 7 consecutive days. Following killing, biomarkers of hepatic and renal toxicities, antioxidant enzyme levels, myeloperoxidase activity, nitric oxide levels, reactive oxygen and nitrogen species (RONS), and lipid peroxidation (LPO) were analyzed spectrophotometrically. Further, the concentration of tumor necrosis factor alpha (TNF-α) was assessed using enzyme-linked immunosorbent assay, and hematological indices: white blood cells (WBC), lymphocytes, and neutrophils and eosinophil counts. Results indicated that DCF-induced increases in biomarkers of hepatic and renal toxicity were significantly ( p < 0.05) lessened in serum of rats co-exposed to DCF and Sel in a dose-dependent manner. DCF mediated decrease in antioxidant status, and increases in RONS, LPO, and TNF-α levels were reduced ( p < 0.05) in the liver and kidney of rats co-exposed to DCF and Sel. Additionally, Sel reduced hematological abnormalities associated with DCF treatment. Light microscopic examination showed that the severity of histopathological lesions induced by DCF was lessened in rats co-exposed to DCF and Sel. Taken together, Sel supplementation mitigated DCF-induced oxidative stress, inflammation, and hematological abnormalities in the liver and kidney of treated rats.

Cinnamon Aqueous Extract Attenuates Diclofenac Sodium and Oxytetracycline Mediated Hepato-Renal Toxicity and Modulates Oxidative Stress, Cell Apoptosis, and Inflammation in Male Albino Rats

“…Antioxidant defense system has a critical role in the protection of cells from reactive oxygen species (ROS) mediated oxidative injury [ 5 ]. Our results showed significantly elevated MDA and NO levels with lower GSH, CAT, and SOD activities of liver and kidney isolated from DFS + OTC, OTC, and DFS treated rats compared to the control rats.…”

“…Similarly, Boshra and Hussein [ 48 ] announced that administration of a single dose of DFS (150 mg/kg body weight) to albino rats caused decrease in hepatic and renal GSH, SOD, and catalase that suggested liver and renal toxicity. The mechanism of DFS-induced oxidative damage in the liver and kidney of treated rats is due to sweeping the antioxidant activities of SOD, CAT, GST, and GSH, enhancing ROS production and deteriorating lipid peroxidation [ 5 ]. Further, similar to our study, increased levels of serum and hepatic lipid peroxidation products and decreased antioxidant levels (SOD, catalase, and glutathione peroxidase) were noticed in OTC intoxicated rats (200 mg/kg body weight/day) for 15 days [ 49 ].…”

“…It is extensively consumed for the management of many chronic conditions such as rheumatoid arthritis, osteoarthritis, ankylosing spondylitis [ 3 ]. DFS elicits its action by hindering the formation of prostaglandin through suppressing cyclooxygenase-1 (Cox-I) and cyclooxygenase-2 (Cox-II) enzymes with the same potency [ 4 ].The presence of DFS as an over-the counter drug may lead to its abuse resulting in threatening deleterious effects on the liver, kidney, and gastrointestinal tract [ 5 ]. The misuse of DFS has been contributed to gastrointestinal problems [ 6 ], hepatotoxicity [ 7 , 8 , 9 ], nephrotoxicity [ 10 ], and neurotoxicity [ 11 ].…”

Selenium attenuates diclofenac‐induced testicular and epididymal toxicity in rats

“…Experimental rats were randomly assigned to five groups (10 rats each), and 0.25 mg/kg selenium was administered following 10 mg/kg diclofenac administration by oral gavage for 14 days. The doses of diclofenac and selenium in the present investigation were selected with references to previously published studies (Adesiyan, Oyejola, Abarikwu, Oyeyemi, & Farombi, 2011; Adeyemi & Olayaki, 2018; Aycan et al., 2018; Owumi & Dim, 2019a, 2019b). The stock solution of diclofenac and selenium were reconstituted in distilled water before administration to experimental animals daily.…”

“…Glutathione S ‐transferase (GST) and glutathione peroxidase (GPx) activities were measured as described by Habig, Pabst, and Jakoby, (1974) and Rotruck et al., (1973) respectively. Reactive oxygen and nitrogen species (RONS), lipid peroxidation (LPO) and glutathione (GSH) were measured as earlier described by Owumi and Dim (2019a), Owumi and Dim (2019b), Farombi, Tahnteng, Agboola, Nwankwo, and Emerole, (2000), Jollow, Mitchell, Zampaglione, and Gillette, (1974) correspondingly. Apart from CAT and SOD assays performed with a UV‐VIS 752S Spectrophotometer, analyses of biochemical endpoints were performed with the aid of plate reader SpectraMax‐384 (Molecular Devices).…”