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More recently this view has been challenged by the discovery of several regulated non-apoptotic cell death pathways activated in specific disease states, including poly(ADP-ribose) polymerase-1 (PARP-1) and apoptosis inducing factor 1 (AIF1)-dependent parthanatos, caspase-1-dependent pyroptosis and receptor interacting protein kinase 1 (RIPK1)-dependent necroptosis (Bergsbaken et al., 2009

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Although ROS participate in signaling pathways of redox processes, they can also be responsible for cell damage, necrosis, or apoptosis, as a consequence of the oxidation process of macromolecules such as lipids, proteins, nuclear DNA, and mitochondrial DNA (Tezel, 2006

The analysis aimed to estimate (1) breed-type differences at baseline (SG-NE vs FG-NE), (2) within-breed responses to the enrichment factor (SG-E vs SG-NE, FG-NE vs FG-E) and (3) between-breed responses to the enrichment factor (breed-type-specific responses)

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