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

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.

Induction of preneoplastic altered hepatic foci following dietary sulphur supplementation

Sulphur is an essential micronutrient required by the body in low concentrations, but its high intake can lead to a serious health hazard. Sulphur compounds are reported to induce several toxic responses in animals, but so far no reports are available on the toxic effects of elemental sulphur, following dietary supplementation. The present investigation was carried out with the aim of providing an insight into the role of dietary supplementation of sulphur on the induction of altered hepatic foci (AHF) using medium term liver bioassay in Wistar rats. Induction of AHF are early neoplastic changes in rat liver in diethylnitrosamine (DEN)-initiated and 2-acetylamino fluorene (2-AAF)-promoted hepatocarcinogenesis. The role of sulphur on induction of AHF was evaluated by the development of negative enzymatic foci for alkaline phosphatase (AlkPase), adenosine triphosphatase (ATPase), glucose-6-phosphatase (G-6-Pase) and positive foci for marker enzymes, glutamyl transferase (GGT), placental isozyme of glutathione-S transferase (GST-P). A significant dose-dependent decrease in the relative and absolute liver weight of sulphur-administered rats was recorded. Dietary supplementation of 2% and 4% sulphur significantly induces both negative and positive focal areas in terms of area and counts for AHF. However, 1% sulphur administration failed to induce AHF up to significant levels. The results thus revealed the possible tumorigenic risk associated with the high sulphur-containing diet.

Enhancing effects of mustard oil on preneoplastic hepatic foci development in Wistar rats

Dietary habits are known to be the major contributory factor in the development of cancer. Mustard oil, which is extensively used in India and elsewhere as a frying and cooking medium, is reported to induce an inflammatory response. The development of altered hepatic foci is an early carcinogenic change in rat liver in diethylnitrosamine (DEN)-induced hepatocarcinogenesis. In the present study, the development of preneoplastic lesions was observed following administration of mustard oil (0.5 mL/day for 8 weeks) in DEN-initiated and partially hepatomized Wistar rats. A significant decrease in the relative and absolute liver weight of mustard oil-exposed rats was recorded. The results revealed a significant increase in the number and area of placental glutathione S-transferase (GST-P) and g-glutamyl transpeptidase (GGT)-positive foci in mustard oil-administered animals. The GST-P and GGT-positive foci were more prominent in the animals given boiled (up to 3008C for 3 hours) mustard oil in comparison to the animals given fresh mustard oil. These results indicate the possible tumourigenic risk associated with mustard oil consumption.