RESUMO
Breaded chicken coated in whey protein isolate (WPI) has been shown to reduce oil absorption during batch frying. What is not known is how this is affected by repeated fryings and whether antioxidant-rich oil will enhance this effect. The objective of this research was to determine how successive daily frying of WPI-coated breaded chicken in antioxidant-rich oil affects oil quality and oil inhibition, moisture retention, color, and texture of the breaded chicken. Chicken fritters with and without a 10% WPI post-breading dip were fried successively for 6 h per day over five days in oil without antioxidant or with either 1000 ppm rosemary extract or propyl gallate. The control oil became spent at 12 h of frying (>24% TPM, <50% DEGLEV). During this time, the oils treated with antioxidants were significantly less spent, and the WPI-treated fritters fried in these oils exhibited 22-49% less lipid; retained 10-18% more moisture; and became darker, less red, and less yellow (lower L*, a*, and b* values) compared to the un-dipped fritters fried in the control oil. These results suggest that the presence of antioxidants in the frying oil mitigated some of the degradative changes in the oil during frying but likely did not play a major role in moisture retention or inhibition of oil absorption.
RESUMO
Zinc is a vital transition metal for Streptococcus pneumoniae, but is deadly at high concentrations. In S. pneumoniae, elevated intracellular free Zn levels result in mis-metallation of key Mn-dependent metabolic and superoxide detoxifying enzymes resulting in Zn intoxication. Here, we report our identification and characterization of the function of the five homologous, CiaRH-regulated Ccn sRNAs in controlling S. pneumoniae virulence and metal homeostasis. We show that deletion of all five ccn genes (ccnA, ccnB, ccnC, ccnD, and ccnE) from S. pneumoniae strains D39 (serotype 2) and TIGR4 (serotype 4) causes Zn hypersensitivity and an attenuation of virulence in a murine invasive pneumonia model. We provide evidence that bioavailable Zn disproportionately increases in S. pneumoniae strains lacking the five ccn genes. Consistent with a response to Zn intoxication or relatively high intracellular free Zn levels, expression of genes encoding the CzcD Zn exporter and the Mn-independent ribonucleotide reductase, NrdD-NrdG, were increased in the ΔccnABCDE mutant relative to its isogenic ccn+ parent strain. The growth inhibition by Zn that occurs as the result of loss of the ccn genes is rescued by supplementation with Mn or Oxyrase™, a reagent that removes dissolved oxygen. Lastly, we found that the Zn-dependent growth inhibition of the ΔccnABCDE strain was not altered by deletion of sodA, whereas the ccn+ ΔsodA strain phenocopied the ΔccnABCDE strain. Overall, our results indicate that the Ccn sRNAs have a crucial role in preventing Zn intoxication in S. pneumoniae.
