Carnosine prevents oxidative damage in porcine muscle cells

Citation

Palin, M.F., Gariépy, C., Beaudry, D., Lapointe, J. and Kalbe, C. (2018) Carnosine prevents oxidative damage in porcine muscle cells. Canadian Meat Council's 98th Annual Conference, May 29-31, 2018, Montreal, Quebec.

Résumé

Meat’s nutrition credentials – high quality protein, bioavailable iron and zinc, and other nutrients required for good health – are well known. Relatively unknown is carnosine, a muscle protective dipeptide that can inhibit the thermal formation of many toxic compounds including 4-Hydroxynonenal (HNE), Malondialdehyde (MDA) and Advanced-Glycation End products (AGEs). Understanding the effect of dietary carnosine in meat models differing in fat content and cooked under different conditions could further enhance its health image.
Ground pork prepared with two levels of carnosine (High; HCAR vs Low; LCAR), fat (HFat; 10% vs LFat; 1.3%) and cooking conditions (HT0; 900C/30min vs LT0; 650C/15min) was digested in vitro mimicking human salivary, gastric and duodenal phases. Digests collected from each phase were analyzed for carnosine, protein carbonyls, free thiols, MDA, HNE, Hexanal and Carboxymethyl-Lysine (CML) as AGEs marker. Partial results are presented.
Carnosine in cooked samples before digestion was 350mg/100g and 438mg/100g for LCAR and HCAR, respectively. In duodenum, single effect of HFat increased MDA (P<0.0001) and CML (P<0.0001). However, a Fat x Carnosine interaction indicated a superior inhibiting effect of HCAR in the LFat group for MDA (P<0.02) and in the HFat group for CML (P<0.01). The pro-oxidant effect of HT0 on increased CML (P<0.0009) was also counteracted by the HCAR (P<0.0001). Carnosine measured after duodenal digestion was 24% higher in HCAR. Increasing carnosine in meat could alleviate the negative effects of high intensity cooking, reduce both protein and lipid oxidation and increase the amount of bioavailable carnosine for additional in situ consumer protection.