Additive Effects of High Fructose Corn Syrup (HFCS) in Experimental Oral Carcinogenesis

Abstract

Pharmacognosy Research,2023,15,4,819-830.DOI:10.5530/pres.15.4.087Published:October 2023Type:Original ArticleAuthors:Kavitha Kalimuthu, Sindhu Ganapathy, Balamurugan Elumalai, Asha Kumarasamypillai Radha Thayammal, Veeran Veeravarmal, and Vijayalakshmi Annamalai Author(s) affiliations:Kavitha Kalimuthu1, Sindhu Ganapathy1,2,*, Balamurugan Elumalai1, Asha Kumarasamypillai Radha Thayammal3, Veeran Veeravarmal4, Vijayalakshmi Annamalai5 1Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalai Nagar, Chidambaram, Tamil Nadu, INDIA. 2Department of Biochemistry, Government Arts College (Autonomous), Kumbakonam, Tamil Nadu, INDIA. 3Department of Biochemistry, Government Arts College, Paramakudi, Tamil Nadu, INDIA. 4Department of Oral and Maxillofacial Pathology, Rajah Muthiah Dental College and Hospital, Annamalai Nagar, Tamil Nadu, INDIA. 5Plant Head, Galileovasan Offshore and Research and Development Private Limited, Nagapattinam, Tamil Nadu, INDIA. Abstract:Introduction: Nowadays, fructose uses dramatically increased in form of High-Fructose Corn Syrup (HFCS) found in juices and packed food. Sustained fructose utilization is detrimental to long-term human health. Objectives: To assess the additive effects of HFCS during 7,12-Dimethylbenz(a)Anthracene (DMBA)-induced Hamster Buccal Pouch Carcinogenesis (HBPCs) model. Materials and Methods: The animals were separated into eight groups: Group I; vehicle control; Group II (0.5% DMBA); Group III and IV (HFCS 8% and 25%); Group V (Sucrose 10%); Group VI and VII (0.5% DMBA+HFCS 8 and 25%) and VIII group (0.5% DMBA+Sucrose 10%) respectively for 14 weeks. After the 14th week of treatment; the tumor morphology, buccal histopathology, and biochemical markers were measured and compared with carcinogenic control as well as vehicle control. Observations and Results: The buccal pouch of golden Syrian hamsters developed well-differentiated squamous cell carcinoma after getting topical applications of 0.5% DMBA in liquid paraffin three times a week for 14 weeks. Although DMBA treatment alone caused 100% tumor development in hamsters, drinking water administration of HFCS at a concentration of 25%/kg body weight (b.w.) to DMBA-treated hamster greatly accelerated the development of oral tumors. Additionally, during DMBA-induced oral carcinogenesis, HFCS moderatingly increased the lipid peroxidation by-products, decreased the status of enzymatic and non-enzymatic antioxidants, modulated the levels of phase I and phase II detoxification agents, and favored the excretion of carcinogenic metabolite. Conclusion: The present study concludes that the additive effect of HFCS relies on its altered peroxidative and antioxidant function as well as effects on phase I and II detoxification enzymes during DMBA-induced hamster buccal pouch carcinogenesis. Taken together the current study described that HFCS induced oral tumour development. From this study we suggested HFCS usage to be curtailed. Keywords:Antioxidants, Detoxification enzymes, DMBA, Hamsters, HFCS, Lipid peroxidation, Oral cancerView:PDF (704.72 KB)