British Journal of Nutrition

Full Papers

Nutritional Toxicity

Genotoxic and carcinogenic risks associated with the dietary consumption of repeatedly heated coconut oil

Smita Srivastavaa1a2, Madhulika Singha1, Jasmine Georgea1, Kulpreet Bhuia1, Anand Murari Saxenaa2 and Yogeshwer Shuklaa1 c1

a1 Proteomics Laboratory, Indian Institute of Toxicology Research (CSIR), Mahatma Gandhi Marg, Lucknow 226 001, UP, India

a2 Department of Zoology, Lucknow University, Lucknow 226 001, UP, India


Repeated heating of vegetable oils at high temperatures during cooking is a very common cooking practice. Repeated heating of edible oils can generate a number of compounds, including polycyclic aromatic hydrocarbons (PAH), some of which have been reported to have carcinogenic potential. Consumption of these repeatedly heated oils can pose a serious health hazard. The objectives of the present study were to evaluate the genotoxic and carcinogenic risks associated with the consumption of repeatedly heated coconut oil (RCO), which is one of the commonly consumed cooking and frying medium. The PAH were analysed using HPLC in fresh CO, single-heated CO (SCO) and RCO. Results revealed the presence of certain PAH, known to possess carcinogenic potential, in RCO when compared with SCO. Oral intake of RCO in Wistar rats resulted in a significant induction of aberrant cells (P < 0·05) and micronuclei (P < 0·05) in a dose-dependent manner. Oxidative stress analysis showed a significant (P < 0·05) decrease in the levels of antioxidant enzymes such as superoxide dismutase and catalase with a concurrent increase in reactive oxygen species and lipid peroxidation in the liver. In addition, RCO given alone and along with diethylnitrosamine for 12 weeks induced altered hepatic foci as noticed by alteration in positive (γ-glutamyl transpeptidase and glutathione-S-transferase) and negative (adenosine triphosphatase, alkaline phosphatase and glucose-6-phosphatase) hepatospecific biomarkers. A significant decrease in the relative and absolute hepatic weight of RCO-supplemented rats was recorded (P < 0·05). In conclusion, dietary consumption of RCO can cause a genotoxic and preneoplastic change in the liver.

(Received December 09 2009)

(Revised April 19 2010)

(Accepted April 29 2010)

(Online publication August 06 2010)


c1 Corresponding author: Y. Shukla, fax +91 522 2628227, email


Abbreviations: AHF, altered hepatic foci; AlkPase, alkaline phosphatase; ATPase, adenosine triphosphatase; B(a)P, benzo(a)pyrene; CO, coconut oil; DEN, diethylnitrosamine; FCO, fresh CO; G6Pase, glucose-6-phosphatase; GGT, γ-glutamyl transpeptidase; Gr, groups; GST-P, glutathione-S-transferase placental type; LPO, lipid peroxidation; PAH, polycyclic aromatic hydrocarbons; RCO, repeatedly heated CO; ROS, reactive oxygen species; SCO, single-heated CO