ABSTRACT
Growing evidence has indicated that cellular redox status regulates various aspects of cellular function. Oxidative stress can elicit positive responses, such as cellular proliferation or activation, as well as negative responses, such as growth inhibition or cell death. For example, the observation that hydrogen peroxide activates a transcription factor, NFKB, suggests that reactive oxygen intermediates act as one of the intracellular second-messengers (1). In addition, we and others have demonstrated that oxidative agents can modulate cellular responses via activation of protein tyrosine kinases or inactivation of protein tyrosine phosphatases (2). These findings strongly indicate the importance of cellular redox status as a regulator of various cellular functions.
