A laboratory system designed to model acrylamide formation showed that taurine may inhibit the production of the potential carcinogen by about 72 percent.
Researchers from China Agricultural University report their findings in the International Journal of Food Science & Technology.
A role for taurine
Taurine, a derivative of the amino acid cysteine, if found naturally in foods including seafood and meat. It has gained certain notoriety by being used as an ingredient in energy drinks, with some national regulators questioning the safety of the ingredient. Taurine is used in energy drinks because some report it helps boost energy – a claim that was rejected by the European Food Safety Authority (EFSA) recently.
It is known that taurine can participate in the Maillard reaction that produces acrylamide, and therefore may reduce the production of acrylamide.
Indeed, researchers from the Korea University, Namyang Dairy Products Co., and the Korea Food Research Institute reported last year that French fries exposed to a taurine solution prior to frying contained 96 per cent less acrylamide than control fries (Food Research International ).
The new study proposes that the mechanism by which this inhibitory effect occurs is via a reaction between glucose and taurine: Acrylamide is produced during the Maillard reaction of sugar and an amino acid called asparagines.
The Maillard reaction is also responsible for the brown color and tasty flavor of baked, fried and toasted foods.
Using a system comprised of asparagine and glucose, the researchers found that taurine could react with glucose and also that taurine reacted directly with any acrylamide formed.
An increase in the antioxidant activity of the model system was also recorded when taurine was included. “Antioxidant-rich natural extracts are attractive candidates in developing effective inhibitors on acrylamide formation in processed foods
“Therefore, the increased antioxidant activity of Maillard reaction products in the presence of taurine could contribute to the inhibition of acrylamide formation in the asparagine / glucose model system,” they added.
The acrylamide story
Despite being a carcinogen in the laboratory, many epidemiological studies have reported that everyday exposure to acrylamide in food is too low to be of concern.
The compound first hit the headlines in 2002, when scientists at the Swedish Food Administration first reported unexpectedly high levels of acrylamide, found to cause cancer in laboratory rats, in carbohydrate-rich foods.
Since the Swedish discovery a global effort has been underway to amass data about this chemical. More than 200 research projects have been initiated around the world and their findings co-ordinated by national governments, the EU and the United Nations.
A toxicology study reported at the end of 2009 that tolerable intakes of acrylamide should be set at 2.6 micrograms per kilogram of body weight to avoid the cancer risk.
According to findings published in Food and Chemical Toxicology, (doi: 10.1016/j.fct.2009.11.048) this would be equivalent to 182 micrograms for a 70 kg human as a tolerable daily intake (TDI) for carcinogenic levels. The TDI for neurotoxicity was found to be higher, at 40 micrograms per kg per day, or 2,800 micrograms per day for a 70 kg human.
Both levels vastly exceed levels estimated by various national agencies or studies. Health Canada, for example, estimates the average exposure of adults to acrylamide in food to be between 0.3 and 0.4 micrograms per kilogram of body weight per day, while a study from Sweden estimated intakes of about 0.5 micrograms per kilogram of bodyweight. The US Food and Drug Administration (FDA) estimated intakes to be around 0.4 micrograms per kilogram of bodyweight per day.
Source: International Journal of Food Science & Technology
June 2011, Volume 46, Issue 6, Pages 1282–1288
Article first published online: 28 MAR 2011 | DOI: 10.1111/j.1365-2621.2011.02611.x
“Acrylamide–taurine adducts formation as a key mechanism for taurine’s inhibitory effect on acrylamide formation”
Authors: R. Hao, X. Leng, H. Jing