ABSTRACT

ABSTRACT

The objective of this study was to evaluate the effect of the addition of Moringa oleifera Lam. seed flour for partial fat replacement in chicken mortadella on physicochemical characteristics, chemical composition, and lipid oxidation. Four mortadellas were prepared: C (control), T1, T3, and T5 (addition of 1%, 3%, and 5% of moringa seed flour, respectively). T5 mortadella had the lowest lipid content (p < 0.05), whereas C mortadella had the highest (p < 0.05). The addition of 5% of moringa seed flour affected color parameters, leading to an increase in L*, a*, and b* values in comparison with the control. Color changes (ΔE) in T3 and T5 mortadellas were the lowest among the samples during a 90-day storage period at 4 °C. The addition of 3 or 5% of moringa seed flour promoted a reduction in lipid oxidation during storage. Moringa seeds have antioxidant activity and, therefore, have the potential to be used as a natural functional ingredient in meat products. The addition of 3% of moringa seed flour seemed to be ideal for chicken mortadella, as it reduced lipid content and promoted lipid stability without causing noticeable color changes during the 90 days of storage.

Samples of Pectoralis major m. were collected, and an RT-PCR analysis of the a-Ryanodine receptor (a RYR) from chicken mRNA hotspot region spanning aminoacid residues 386 to 540, numbered according to the turkey sequence, revealed two classes of transcripts. The sequences of the first class were similar to turkey and human with 97% and 74% of identity, respectively, and included all transcripts with substitutions in the nucleotide sequence. The second class was characterized by the deletion of nucleotides, leading to a premature stop codon and coding for a truncated and nonfunctional protein. These results are to date the first report related to the sequencing of the chicken αRYR hotspot region 1, which will possibility serve as a guide for further studies regarding a solution in the poultry production chain related to the problem of pale, soft and exudative (PSE) meat.

The biological cause of Pork Stress syndrome, which leads to PSE (pale, soft, exudative) meat, is excessive release of Ca(2+) ions, which is promoted by a genetic mutation in the ryanodine receptors (RyR) located in the sarcoplasmic reticulum of the skeletal muscle cells. We examined the relationship between the formation of PSE meat under halothane treatment and heat stress exposure in chicken alphaRYR hot spot fragments. Four test groups were compared: 1) birds slaughtered without any treatment, i.e., the control group (C); 2) birds slaughtered immediately after halothane treatment (H); 3) birds slaughtered immediately after heat stress treatment (HS), and 4) birds exposed to halothane and to heat stress (H+HS), before slaughtering. Breast muscle mRNA was extracted, amplified by RT-PCR, and sequenced. PSE meat was evaluated using color determination (L* value). The most common alteration was deletion of a single nucleotide, which generated a premature stop codon, resulting in the production of truncated proteins. The highest incidence of nonsense transcripts came with exposure to halothane; 80% of these abnormal transcripts were detected in H and H+HS groups. As a consequence, the incidence of abnormal meat was highest in the H+HS group (66%). In HS, H, and C groups, PSE meat developed in 60, 50, and 33% of the samples, respectively. Thus, halothane apparently modulates alphaRYR gene expression in this region, and synergically with exposure to heat stress, causes Avian Stress syndrome, resulting in PSE meat in broiler chickens.