The Protective Effects of p-Coumaric Acid on Acute Liver and Kidney Damages Induced by Cisplatin

Abstract

In this study, we aimed to investigate the effects of p-Coumaric acid (PCA) on cisplatin (CIS)-induced hepatotoxicity and nephrotoxicity in Wistar adult rats for 24 h compared to untreated control groups. In this experiment, 40 Wistar adult rats were utilized and divided randomly into five groups. After 24 h of CIS administration, liver and kidneys were harvested and assessed by H&E staining. Also, markers for oxidative stress and antioxidants were analyzed in theses tissues. Compared to the control group, accumulation of malondialdehyde was increased in groups treated CIS, whereas superoxide dismutase activities and glutathione levels were distinctly diminished in this group. The study’s histopathological findings such as hydropic degeneration, vascular congestion, sinusoidal dilatation in hepatocytes and tubular necrosis in kidneys were in accordance with the results of markers for oxidative stress. PCA may prevent hepatotoxicity and nephrotoxicity by increased antioxidant enzymes and reduced oxidant parameters.

The antiapoptotic and antioxidant effects of eugenol against cisplatin‐induced testicular damage in the experimental model

“…Testicular dysfunction or damage is among the critical side effects of chemotherapeutic drugs such as cisplatin (Madhu, Reddy, & Reddy, ). Cisplatin‐induced toxicity is consisted by increased formation of reactive oxygen species (ROS) and reduced generation or activity of antioxidant enzymes (Ekinci Akdemir et al, ). ROS formation depends on the dose of cisplatin and the process of its application.…”

“…Cisplatin is a chemotherapeutic agent that is used in the clinical therapy of various types of cancer. But the use of cisplatin is limited due to numerous undesirable side effects such as neurotoxicity (Ekinci‐Akdemir, Gulcin, Gursul, Alwasel, & Bayir, ), nephrotoxicity (Mora, Antunes, Francescato, & Bianchi, ), hepatotoxicity (Ekinci Akdemir, Albayrak, Calik, Bayir, & Gulcin, ) and ototoxicity (Le, Tabuchi, Warabi, & Hara, ), and even testicular toxicity (Reddy, Madhu, & Reddy, ). The testis toxicity mechanism via cisplatin has not been literally identified; however, oxidative stress has been reported among the many physiopathologies.…”

“…The testis toxicity mechanism via cisplatin has not been literally identified; however, oxidative stress has been reported among the many physiopathologies. Numerous researches demonstrated that oxygen derived free radicals raise and the intracellular glutathione is consumed due to cisplatin (Ekinci Akdemir et al, ; Ekinci‐Akdemir et al, ). It is well accepted that antioxidant enzymes such as glutathione peroxidase, superoxide dismutase and catalase are crucial to scavenge the oxygen derived free radical arising from cisplatin‐induced oxidative stress to avoid a possible further damage in cells.…”

Phenolic Acids of Plant Origin—A Review on Their Antioxidant Activity In Vitro (O/W Emulsion Systems) Along with Their in Vivo Health Biochemical Properties

“…p-CA has been reported to decrease the peroxidation of low-density lipoproteins (LDL) and exert anti-mutagenesis, anti-genotoxicity, and anti-microbial activities [117]. Very recently, Ferreira et al (2019) [118] gave a literature overview of certain biochemical properties of CA (including radical scavenging and tumor suppression activities) that link to its claimed pharmacological effects.…”

The toxicological impact of some avermectins on human erythrocytes glutathione S‐transferase enzyme

“…In addition, the properties of GST in prokaryotes seem to be involved in the detoxification of xenobiotics, including antibiotics . GST enzymes have been associated with increased bacterial resistance to several antibiotics, such as tetracycline and rifampicin . The degradation of several antibiotics (tetracycline, sulfathiazole, ampicillin) using microorganisms containing GSTs under immobilized conditions has been reported .…”