Anticarcinogenic Activity of Allylmercaptocaptopril Against Aflatoxin-B1 Induced Liver Carcinoma in Rats

Sharma, Swati; Lakshmi, K. S.; Chitra, V.; Lakshmi, I.; M.Pharm, Mathur P.

doi:10.29333/ejgm/82696

Cited by 3 publications

(3 citation statements)

References 24 publications

(10 reference statements)

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“…HEX levels are important in determining the glycolytic capacity of cancer cells. [ 20 21 ] Increased activities of HEX and PGI during development of tumor cells observed in the present study are in agreement with the finding of earlier study,[ 22 ] wherein the increased activities of glycolytic enzymes have been found to correlate with the degree of malignance in tumor tissues. High levels of HEX reported in Novikoff and Zajdela hepatomas and aflatoxin-B1 induced liver carcinoma[ 22 23 24 ] signify the functional importance of HEX in tumor cells to utilize excess glucose for the production of ATP.…”

Section: Discussionsupporting

confidence: 93%

“…[ 21 ] Decreased rate of glucose-6-phosphatase mediated dephosphorylation is also reported in malignant cells. [ 31 ] Decreased activity of fructose-1,6-bisphosphatase, the key regulatory enzyme for the synthesis of glucose-6-phosphate from pyruvic acid observed in liver of Group III rats is supported by the earlier report,[ 22 ] which reported that in aflatoxin-B1 induced liver carcinoma, there appears to be a decreased fructose-1,6-bisphosphatase in the tumor and consequently a block in the pathway, leading to the synthesis of glucose-6-phosphate from pyruvate.…”

Section: Discussionmentioning

confidence: 56%

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Modulatory role of Shorea robusta bark on Glucose-metabolizing enzymes in diethylnitrosamine induced hepatocellular carcinoma in rats

Kalaiselvan¹,

Anand

Gokulakrishnan

et al. 2015

Phcog Mag

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Introduction:The modulations of glucose-metabolizing enzyme activities play a vital rolein the depletion of energy metabolism and leads to inhibition of cancer growth.Objective:To find the effect of shorearobusta bark extract on glucose-metbolizing enzymes in diethylnitrosamine (DEN) induced hepatocellular carcinoma rats.Materials and Methods:Biochemical evaluation of glucose metabolizing enzyme were done in before and after shorearobusta bark extract (500mg/kg) treatment in DEN induced rats.Results:A significant increasein the activities of the key glycolytic enzymes viz., hexokinase and phosphoglucoisomerase, with a significant decrease in the gluconeogenic enzymes glucose-6-phosphatase and fructose-1,6-bisphosphatasewere observed in HCC bearing rats, when compared with the control. Administration of shorearobusta extract caused a significant decrease in theactivities of glycolytic enzymes and an increase in the gluconeogenic enzymes activities to near normal values.Conclusion:The current findings suggest that the S. robusta extract has a definite modulating role on the key enzymes ofglucose-metabolism in HCC. The modulatory effect may be due to the phytoactive constituents present in the extract of S. robusta.SUMMARY Administration of shorea robusta bark extract caused a significant decrease in the activities of glycolytic enzymes and an increase in the gluconeogenic enzymes activities to near normal values. The S. robusta extract has modulatory activity on the carbohydrate metabolism in DEN-induced HCC bearing rats through a mechanism that which does not provoke any acute biochemical disturbances in the metabolic pathways of glycolysis and gluconeogenesis. The modulatory effect of S. robusta extract may be attributed to the presence of active compounds such as polyphenols and flavonoids. Abbreviations used: HCC: Hepatocellular Carcinoma, SRBE: Shorearobusta bark extract; HEX: Hexokinase; PGI: Phosphoglucoisomerase; DEN: Diethylnitrosamine.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 56%

Modulatory role of Shorea robusta bark on Glucose-metabolizing enzymes in diethylnitrosamine induced hepatocellular carcinoma in rats

Kalaiselvan¹,

Anand

Gokulakrishnan

et al. 2015

Phcog Mag

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“…Our data were supported by other previous findings; Frederiks et al (2008) demonstrated that chemically induced HCC in rats was characterized by increased G6PDH activity. Sharma, Lakshmi, Chitra, Lakshmi, and Pharm (2011) reported an increased aldolase activity in rats with induced HCC. Schlichtholz et al (2005) reported a significant increase in citrate synthase activity in human pancreatic cancer.…”

Section: Discussionmentioning

confidence: 98%

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

El-Bahrawy¹,

El-Ashmawy²,

Shamloula³

et al. 2014

IJB

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Incidence of hepatocellular carcinoma (HCC) has increased sharply in the last 10 years, with an especially high incidence in Egypt. This study was conducted to evaluate the impact of unbalanced diets on liver tumor through investigation of some biochemical mediators/pathways implicated in the pathogenesis of HCC. Male albino mice were divided into two major groups: Control group and Hepatocellular carcinoma (HCC) group; each group was further divided into four subgroups according to received diet: high fat (HF), low fat (LF), high carbohydrate (HC), and low carbohydrate (LC) groups. The results indicated that induction of HCC in mice showed marked body weight loss. Liver sections of HCC groups showed malignant giant cells and strong expression of p53. HCC mice groups kept on HF and LC diets showed the lowest survival rate, a significant increase in glucose-6-phosphate dehydrogenase (G6PDH), aldolase, and citrate synthase activities, a significant increase in serum E-cadherin as well as a significant decrease in insulin-like growth factor-1 (IGF-1) compared with LF diet. These results suggest that the molecular pathogenesis of HCC in mice correlates reduction of serum IGF-1 and elevated serum E-cadherin accompanied by reprogrammed metabolic profile shifted towards increased glycolysis and lipogenesis. These pathogenic changes were enhanced by over-consumption of carbohydrates, fats, and proteins, whereas dietary fat restriction could have a protective/ameliorative effect against the incidence of HCC.

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Biochemical/metabolic changes associated with hepatocellular carcinoma development in mice

et al. 2014

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Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality after lung and stomach cancers. This work was undertaken to investigate some of the biochemical mediators/pathways associated with or implicated in the pathogenesis of HCC. Male albino mice were classified into two groups: normal control group and HCC group. Early stage HCC was induced by injection of diethylnitrosamine (DEN) i.p. 200 mg/kg as a single dose, and after 2 weeks, the mice were given i.p. injection of thioacetamide (TAA) 100 mg/kg twice per week for 4 weeks. Mice were left for further 2 weeks without any treatment, after which, mice were sacrificed; blood and liver samples were collected. Serum was used for determination of activities of glucose-6-phosphate dehydrogenase (G6PDH) and aldolase as well as levels of insulin-like growth factor-1 (IGF-1) and epithelial cadherin (E-cadherin). One portion of the liver was used for histopathological examination and immunohistochemical staining of the tumor suppressor p53 protein. Another portion of the liver was used for determination of citrate synthase activity. Induction of HCC in mice resulted in significant increase in G6PDH and aldolase activities, and E-cadherin level, but significant decrease in IGF-1. HCC mice group showed moderate expression of p53 protein. These results suggest that the molecular pathogenesis of HCC in mice involves reduction of serum level of IGF-1 and increased serum level of E-cadherin accompanied by dysregulation of p53 protein expression. HCC was also associated with reprogrammed metabolic profile shifted toward increased glycolysis and lipogenesis.

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Anticarcinogenic Activity of Allylmercaptocaptopril Against Aflatoxin-B1 Induced Liver Carcinoma in Rats

Abstract: Aim

Cited by 3 publications

References 24 publications

Modulatory role of Shorea robusta bark on Glucose-metabolizing enzymes in diethylnitrosamine induced hepatocellular carcinoma in rats

Modulatory role of Shorea robusta bark on Glucose-metabolizing enzymes in diethylnitrosamine induced hepatocellular carcinoma in rats

Effect of Diet Intake Imbalance in Hepatocellular Carcinoma Progression

Biochemical/metabolic changes associated with hepatocellular carcinoma development in mice

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