Genetic parameter estimates for plasma oxidative status traits in slaughter pigs

The aim of the present study was to assess the effect of sex and to estimate genetic parameters for several traits related to plasma oxidative status in slaughter pigs, i.e., ferric reducing ability of plasma (FRAP), concentrations of a-tocopherol and malondialdehyde (MDA), and glutathione peroxidase (GPx) activity. Blood samples were collected at slaughter from 477 Pietrain x (Landrace x Large White intercross) pigs of 2 performance test stations. Heritabilities (+/- SE) of plasma oxidative status traits as well as their phenotypic and additive genetic correlations with animal performance traits were estimated with multiple-trait REML animal models using VCE software. Results displayed no significant difference between barrows and gilts for FRAP and alpha-tocopherol in plasma. However, gilts had a significantly higher concentration of MDA and lower GPx activity compared with barrows. Heritability estimates were high for GPx (0.55 +/- 0.05), and medium to low for alpha-tocopherol (0.30 +/- 0.06), FRAP (0.22 +/- 0.05), and MDA (0.15 +/- 0.04). Estimated additive genetic and phenotypic correlations between these four traits were generally low, except for a negative additive genetic correlation between FRAP and GPx of -0.45 (+/- 0.23). Additive genetic correlations between plasma oxidative status traits and animal performance traits were also generally absent or low with maximum values of similar to 0.3. Parameter estimates in this study have to be interpreted with caution because of the small size of the dataset. Nevertheless, it may be concluded that there is considerable additive genetic variance for plasma oxidative status traits in slaughter pigs. More research is warranted on the genetic determination of oxidative stress in farm animals and its relevance in breeding programs

Mechanisms linking colorectal cancer to the consumption of (processed) red meat : a review

Colorectal cancer (CRC) is the third most commonly diagnosed cancer in the world. The vast majority of CRC cases have been linked to environmental causes rather than to heritable genetic changes. Over the last decades, epidemiological evidence linking the consumption of red and, more convincingly, of processed red meat to CRC has accumulated. In parallel, hypotheses on carcinogenic mechanisms underlying an association between CRC and the intake of red and processed red meat have been proposed and investigated in biological studies. The hypotheses that have received most attention until now include (1) the presence of polycyclic aromatic hydrocarbons and heterocyclic aromatic amines, two groups of compounds recognized as carcinogenic, (2) the enhancing effect of (nitrosyl)heme on the formation of carcinogenic N-nitroso compounds and lipid peroxidation. However, none of these hypotheses completely explains the link between red and processed red meat intake and the CRC risk. Consequently, scientists have proposed additional mechanisms or refined their hypotheses. This review first briefly summarizes the development of CRC followed by an in-depth overview and critical discussion of the different potential carcinogenic mechanisms underlying the increased CRC risk associated with the consumption of red and processed red meat