Abstract
Abstract Introduction: Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide. In this study Gatifloxacin an antimicrobial drug which has been banned due to some serious adverse effects evaluated for the other pharmacological activities. Data from the present investigation suggest that Gatifloxacin suppresses the tumors and decrease the biochemical markers which are elevated in HCC. Objective: This study is an attempt to evaluate the potential chemopreventive influence of Gatifloxacin in hepatocarcinogenic rats. Hepatocarcinogeneis was induced by a single intraperitoneal injection of diethylnitrosamine (DENA) in phosphate buffer (200 mg/kg). Results and conclusion: Experimental animals exposed to DENA caused a significant alteration in serum indices of liver enzymes glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), acid phophatase (AP), total cholesterol (TC), triglycerides (TG) and high density lipoproteins (HDL), total proteins (TPR) and blood glucose level in tested animals. Results also revealed severe histological and immunohistochemical changes in hepatic tissues. These included disorganized hepatic parenchyma, appearance of pseudoacinar and trabecular arrays of hepatocytes and alterations in alpha fetoprotein (AFP) levels. Administration of Gatifloxacin relatively improved the biochemical parameters to values approximating those of the normal controls. SGOT, SGPT, ALP, level was significantly decreased (p<0.001, p<0.01, p<0.001 respectively) in therapeutic control while TPR, ALB level was significantly increased (p<0.001, p<0.001 respectively) and delayed the initiation of carcinogenesis. Rats treated with Gatifloxacin only showed altered levels of liver enzymes, arrhythmic symptoms and abdominal fat deposition. In conclusion, DENA significantly changes the biological enzymatic activities in serum and the integrity of hepatic tissues. Hence, Gatifloxacin proved to possess the potential for the treatment of hepatocellularcarcinomas in rats exposed to DENA.
Highlights
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide
Experimental animals exposed to DENA caused a significant alteration in serum indices of liver enzymes glutamate oxaloacetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), alkaline phosphatase (ALP), acid phophatase (AP), total cholesterol (TC), triglycerides (TG) and high density lipoproteins (HDL), total proteins (TPR) and blood glucose level in tested animals
Gatifloxacin proved to possess the potential for the treatment of hepatocellularcarcinomas in rats exposed to DENA
Summary
Hepatocellular carcinoma (HCC) is a major cause of cancer death worldwide. In this study Gatifloxacin an antimicrobial drug which has been banned due to some serious adverse effects evaluated for the other pharmacological activities. Of which hepatocellular carcinoma (HCC) is the predominant type, is a major cause of cancer death worldwide [1], accounts for about 90% of all cases of liver cancer and is the fourth most common cause of cancer mortality [2]. Primary sources of human exposure to nitrosamines are agricultural, pharmaceutical and tobacco products, cosmetics and food preservatives [4]. DENA is metabolized to its active ethyl radical, which interacts with DNA causing mutation and subsequent oncogenesis [7]
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