Abstract
Zinc deficiency causes oxidative stress in many organisms including the yeast Saccharomyces cerevisiae. Previous studies of this yeast indicated that the Tsa1 peroxiredoxin is required for optimal growth in low zinc because of its role in degrading H2O2. In this report, we assessed the importance of other antioxidant genes to zinc-limited growth. Our results indicated that the cytosolic superoxide dismutase Sod1 is also critical for growth under zinc-limiting conditions. We also found that Ccs1, the copper-delivering chaperone required for Sod1 activity is essential for optimal zinc-limited growth. To our knowledge, this is the first demonstration of the important roles these proteins play under this condition. It has been proposed previously that a loss of Sod1 activity due to inefficient metallation is one source of reactive oxygen species (ROS) under zinc-limiting conditions. Consistent with this hypothesis, we found that both the level and activity of Sod1 is diminished in zinc-deficient cells. However, under conditions in which Sod1 was overexpressed in zinc-limited cells and activity was restored, we observed no decrease in ROS levels. Thus, these data indicate that while Sod1 activity is critical for low zinc growth, diminished Sod1 activity is not a major source of the elevated ROS observed under these conditions.
Highlights
Zinc is an essential nutrient because it is a required structural or catalytic cofactor for many proteins
We previously observed that zinc-deficient yeast experience increased oxidative stress and that the Tsa1 peroxiredoxin is required to deal with this oxidative stress and allow for optimal growth under zinc-limiting conditions [13]
These results raised the question of whether Tsa1 was uniquely important in this role or whether other antioxidant genes were important for low zinc growth
Summary
Zinc is an essential nutrient because it is a required structural or catalytic cofactor for many proteins These proteins include zinc finger-containing transcription factors and enzymes such as carbonic anhydrase, alcohol dehydrogenase, and Cu/Zn-superoxide dismutase. Mechanisms of zinc homeostasis are required to maintain intracellular zinc levels within a narrow optimal range Both extremes of zinc status, i.e. excess and deficiency, cause oxidative stress in cells through the increased accumulation of reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, and hydroxyl radical [1,2]. The oxidative stress of zinc deficiency leads to increased levels of DNA damage [8,9,10] For these reasons, zinc deficiency has been proposed to be an important risk factor for cancer and other human diseases [5,11]. It has been estimated that ,2 billion people worldwide do not consume adequate levels of zinc in their diets so zinc deficiency is clearly an important public health problem [12]
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