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Interestingly, NAC treatment significantly reduced the lung bacterial burden of Mtb-infected mice in both wild-type and gp91 Phox/ mouse macrophages, suggesting that the antimycobacterial effect of NAC is not entirely dependent on NAPDH-induced ROS production within macrophages (154)

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Reduction in cellular energy (ATP) content, as one of the mechanisms for IRI, leads to destroy cellular ion homeostasis with activation of hydrolases and damage of elective permanence of cell membranes and cause of decrease in organ function after transplantation and limit in survival of transplanted organs (23) (Figure 2)