Chilling injury, mechanisms

Lipid oxidation has been proposed as the vehicle for manifestation of injury and loss of quality in food by physiological stresses such as chilling injury, senescence and dehydration. The objective of this chapter is to review how localized degradation of antioxidants has been used as a marker for early detection of lipid oxidation as well as in defining the mechanism of oxidative challenge. 

Toxicities included an infusion reaction consisting of fever, chills, pain, asthenia, nausea, and vomiting. This syndrome was typically observed after the initial infusion, was self-limited, and frequently did not recur with subsequent infusions. The most serious toxicity was cardiac dysfunction, defined as clinical findings of congestive heart failure and/or subclinical declines in cardiac ejection fraction, which was seen in 5% of patients. Cardiotoxicity was unanticipated, as it had not been detected in previous studies. The mechanism for this effect is unclear, but is likely related to trastuzumab s antiproferative effect on HER2-mediated homeostasis and response to injury. 

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