High temperatures can negatively affect plant growth and productivity. It is known that heat stress induces significant changes in normal physiological processes and generates reactive oxygen species (ROS). In order to limit the oxidative damage, occurring under stress, plants have developed detoxification systems, able to scavenge the highly toxic ROS. In order to clarify the relationship between cell growth, redox homeostasis and activation of defence mechanisms, the effect of moderate heat stress (exposure to 35°C) has been studied in tobacco BY-2 cells. The data indicates that the block of the cell cycle is an initial defence strategy. A strong increase in the expression of HSPs and an enhancement of antioxidant enzymes also occurs. However, these defence mechanisms seems to be not sufficient to cope with a persistent heat stress. Five-seven days after the start of heat treatment, the activity of antioxidant enzymes declines. The parallel increase in ROS determines oxidative damages and cell death. Interestingly, the pre-treatment of BY-2 cells with antioxidants correlates with a better growth capability, due to the recovery of cell divisions and a decrease in cell death.

An increase in antioxidants helps tobacco BY-2 cells to overcome moderate heat stress

DIPIERRO, NUNZIO;DIPIERRO, Silvio;DE PINTO, MARIA CONCETTA
2012-01-01

Abstract

High temperatures can negatively affect plant growth and productivity. It is known that heat stress induces significant changes in normal physiological processes and generates reactive oxygen species (ROS). In order to limit the oxidative damage, occurring under stress, plants have developed detoxification systems, able to scavenge the highly toxic ROS. In order to clarify the relationship between cell growth, redox homeostasis and activation of defence mechanisms, the effect of moderate heat stress (exposure to 35°C) has been studied in tobacco BY-2 cells. The data indicates that the block of the cell cycle is an initial defence strategy. A strong increase in the expression of HSPs and an enhancement of antioxidant enzymes also occurs. However, these defence mechanisms seems to be not sufficient to cope with a persistent heat stress. Five-seven days after the start of heat treatment, the activity of antioxidant enzymes declines. The parallel increase in ROS determines oxidative damages and cell death. Interestingly, the pre-treatment of BY-2 cells with antioxidants correlates with a better growth capability, due to the recovery of cell divisions and a decrease in cell death.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11586/116151
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