Abstract
H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells is mediated by reactive carbonyl species (RCS), degradation products of lipid peroxides, which activate caspase-3-like protease (C3LP). Here, we investigated the mechanism of RCS accumulation in the H2O2-induced PCD of BY-2 cells. The following biochemical changes were observed in 10-min response to a lethal dose (1.0 mM) of H2O2, but they did not occur in a sublethal dose (0.5 mM) of H2O2. (1) The C3LP activity was increased twofold. (2) The intracellular levels of RCS, i.e., 4-hydroxy-(E)-hexenal and 4-hydroxy-(E)-nonenal (HNE), were increased 1.2–1.5-fold. (3) The activity of a reduced nicotinamide adenine dinucleotide phosphate (NADPH)-dependent carbonyl reductase, scavenging HNE, and n-hexanal was decreased. Specifically, these are the earliest events leading to PCD. The proteasome inhibitor MG132 suppressed the H2O2-induced PCD, indicating that the C3LP activity of the β1 subunit of the 20S proteasome was responsible for PCD. The addition of H2O2 to cell-free protein extract inactivated the carbonyl reductase. Taken together, these results suggest a PCD-triggering mechanism in which H2O2 first inactivates a carbonyl reductase(s), allowing RCS levels to rise, and eventually leads to the activation of the C3LP activity of 20S proteasome. The carbonyl reductase thus acts as an ROS sensor for triggering PCD.
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Claims 8
Claim · model-written summary
The C3LP activity increased twofold after a lethal dose of H2O2 but not after a sublethal dose in BY-2 cells.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e1“The following biochemical changes were observed in 10-min response to a lethal dose (1.0 mM) of H2O2, but they did not occur in a sublethal dose (0.5 mM) of H2O2. (1) The C3LP activity was increased twofold”
Claim · model-written summary
Intracellular RCS levels (4-hydroxy-(E)-hexenal and HNE) increased 1.2–1.5-fold after a lethal dose of H2O2 in BY-2 cells.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e1“The following biochemical changes were observed in 10-min response to a lethal dose (1.0 mM) of H2O2, but they did not occur in a sublethal dose (0.5 mM) of H2O2. (1) The C3LP activity was increased twofold”
e2“The intracellular levels of RCS, i.e., 4-hydroxy-(E)-hexenal and 4-hydroxy-(E)-nonenal (HNE), were increased 1.2–1.5-fold”
Claim · model-written summary
NADPH-dependent carbonyl reductase activity decreased after a lethal dose of H2O2 in BY-2 cells.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e1“The following biochemical changes were observed in 10-min response to a lethal dose (1.0 mM) of H2O2, but they did not occur in a sublethal dose (0.5 mM) of H2O2. (1) The C3LP activity was increased twofold”
e3“The activity of a reduced nicotinamide adenine dinucleotide phosphate (NADPH)-dependent carbonyl reductase, scavenging HNE, and n-hexanal was decreased”
Claim · model-written summary
The proteasome inhibitor MG132 suppressed H2O2-induced PCD in BY-2 cells.
- Taxon
- tobacco Bright Yellow-2 (BY-2) cellse0
- Treatment
- proteasome inhibitor MG132e4
- Outcome
- H2O2-induced PCDe4
- Direction
- suppressede4
Not reportedComparator
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e4“The proteasome inhibitor MG132 suppressed the H2O2-induced PCD”
Claim · model-written summary
The C3LP activity of the beta1 subunit of the 20S proteasome is responsible for PCD in BY-2 cells.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e5“indicating that the C3LP activity of the β1 subunit of the 20S proteasome was responsible for PCD”
Claim · model-written summary
H2O2 added to cell-free protein extract inactivated the carbonyl reductase.
- Taxon
- tobacco Bright Yellow-2 (BY-2) cellse0
- Treatment
- The addition of H2O2 to cell-free protein extracte6
- Gene
- carbonyl reductasee6
- Outcome
- carbonyl reductasee6
- Direction
- inactivatede6
Not reportedComparator
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e6“The addition of H2O2 to cell-free protein extract inactivated the carbonyl reductase”
Claim · model-written summary
The authors propose that H2O2 inactivates a carbonyl reductase, letting RCS rise and activating C3LP activity of the 20S proteasome, which triggers PCD.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e7“Taken together, these results suggest a PCD-triggering mechanism in which H2O2 first inactivates a carbonyl reductase(s), allowing RCS levels to rise, and eventually leads to the activation of the C3LP activity of 20S proteasome”
Claim · model-written summary
The carbonyl reductase acts as an ROS sensor for triggering PCD in BY-2 cells.
Verbatim
e0“H2O2-induced programmed cell death (PCD) of tobacco Bright Yellow-2 (BY-2) cells”
e2“The carbonyl reductase thus acts as an ROS sensor for triggering PCD”