The ameliorative effect of Vitamin C in experimentally induced colon cancer in rats

Abstract

The present study was designed to investigate the ameliorative effect of vitamin C administration on serum alanine aminotransferase (ALT),aspartate aminotransferase(AST),Urea, Creatinine, Alphafetoprotein(AFP), Carcinoembryonic antigen (CEA) and carbohydrate antigen 19.9 (CA 19-9), in addition to tumor necrosis factor alpha (TNF-α) , Cytochromep4502E1 and Caspase-9 gene expression in colon cancer induced by 1,2-dimethylhydrazine (DMH)in rats. Forty white female albino rats were divided into four equal groups (10 each). Group I(control group):received no drugs. Group II:(DMH group): rats injected subcutaneously with DMH (35 mg/kg body weight),twice a week for 5 consecutive weeks for colon cancer induction. Group III:(protective group): rats administrated vit C(200 mg kg-1 b. wt) orally and for 4 weeks before DMH injection and continued with vit C administration daily till the end of the experiment .Group IV:(treatment group):rats injected subcutaneously with DMH then administrated Vit C for 6 weeks till the end of the experiment. Blood and colon tissue samples were collected from all animal groups at the end of the experiment. The obtained results showed that DMH injection to rats significantly increased serum(ALT, AST, Urea, Creatinine, AFP, CEA, CA 19-9) and colon tissue TNF-α and CYP2E1while colon tissue caspase-9 gene wassignificantly decreasedwhen compared to control.Administration of Vit C significantly decreased serum (ALT, AST, Urea, Creatinine, AFP, CEA, CA 19-9) in addition to TNF-α and CYP2E1in colon tissue. How every, caspase-9 gene expression showed a significant increase. Histopathological examination of colon tissue edesquamation of the colon epithelium with heavy leukocytic infiltrationin DMH group. While administration of vitamin C in colon cancer induced rats showed mild destruction of the lining epithelium with mild leukocytic infiltration in addition to mild malignancy of epithelium when compared to DMH group. These results indicated the protective effect of Vit C against DMH induced colon cancer.

The Antioxidant and Antitumor Efficiency of Litophyton sp. Extract in DMH-Induced Colon Cancer in Male Rats

“…The increased levels of serum cholesterol and triglycerides observed after DMH injection are consistent with those reported by Abdel-Hamid et al [ 19 ]. They stated that the serum triglycerides concentration is positively associated with bile acid synthesis, which may promote carcinogenesis in the large intestine.…”

“…The increased levels of pro-inflammatory cytokines (TNF-& IL-1β), and tumor markers (CEA, CA19.9 and AFP) matched with a decrease in apoptotic biomarkers (CD4+) in colon cancer-bearing rats are in line with other earlier research [ 1 , 4 , 19 ]. Reactive oxygen species (ROS) production significantly contributes to oxidant/antioxidant imbalance.…”

Evaluation of membrane-destructive processes in rats with induced carcinogenesis of the colon using the cytostatic vincristine

“…Elevated urea levels also indicate changes in liver function. Urea is the end product of protein metabolism, the content of which in the serum of experimental animals depends on the intensity of its synthesis and excretion [11]. After 30 weeks of DMH administration, the serum urea content of the affected animals increased by 12% relative to the control rat group.…”

“…A number of authors note that hepatocytes are the most sensitive to chemotherapy. Under the action of cytostatics, the integrity of the plasma membranes of liver cells is violated, as a result of progressive cell-hepatic failure and cytolysis of hepatocytes [7,11].…”

Design, Synthesis, and Molecular Docking of Paracyclophanyl-Thiazole Hybrids as Novel CDK1 Inhibitors and Apoptosis Inducing Anti-Melanoma Agents

“…Human kinases remain interesting targets in oncology; cyclindependent kinases (CDKs) are a class of serine/threonine-protein kinases that regulates the temporal progression of cells through the cell cycle [18]. To date, 21 different CDKs (1−11a and 11b−20) have been identified in the human genome, and they can be classified into two main categories based on their primary roles [19,20]. CDK1, CDK2, CDK4, and CDK6 have been discovered to regulate the cell cycle progression upon binding to cyclin proteins.…”