TNF and infection: Although the oxidative stress generated after the infection is a hallmark of professional phagocytic cells, it has been demonstrated that oxidative stress in nonphagocytic cells is generated by many mechanisms, including dysfunction of mitochondria in infected mice [29] and cardiomyocytes [30] and cytokines signaling like TNF [5], and also by the action of lipoxygenase, cyclooxygenase, and cytochrome P450-dependent oxygenases during arachidonic acid metabolism [31].