The potential role of acrolein in plant ferroptosis-like cell death

Abstract

The iron dependent, programmed cell death, ferroptosis was described first in tumour cells. It showed distinct features from the already known cell death forms such as apoptosis, necrosis and autophagy. The caspase independent cell death could be induced by the depletion of glutathione by erastin or by the inhibition of the lipid peroxide scavenger enzyme GPX4 by RSL3 and it was accompanied by the generation of lipid reactive oxygen species. Recently, ferroptosis-like cell death associated to glutathione depletion, lipid peroxidation and iron dependency could also be induced in plant cells by heat treatment. Unfortunately, the mediators and elements of the ferroptotic pathway have not been described yet. Our present results on Arabidopsis thaliana cell cultures suggest that acrolein, a lipid peroxide-derived reactive carbonyl species, is involved in plant ferroptosis-like cell death. The acrolein induced cell death could be mitigated by the known ferroptosis inhibitors such as Ferrostatin-1, Deferoxamine, α-Tocopherol, and glutathione. At the same time acrolein can be a mediator of ferroptosis-like cell death in plant cells since the known ferroptosis inducer RSL3 induced cell death could be mitigated by the acrolein scavenger carnosine. Finally, on the contrary to the caspase independent ferroptosis in human cells, we found that caspase-like activity can be involved in plant ferroptosis-like cell death.

Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

“…Inducers: erastin [22], sorafenib [23], acrolein [22] Inhibitors: DFO [24], vitamin B12 [25], carvacrol [26], Chinese herbal medicines including naotaifang [27] Inducers: alkylating agents [28], X-rays [29] Inhibitors: Nec-1 [30], infliximab [7], dabrafenib [31], Chinese herbal medicines including curcumin [32] 2 Oxidative Medicine and Cellular Longevity conditions, instead of SLC39A14 which is a member of the solute carrier 39 family mediating cellular uptake of iron, zinc, and manganese [54,55]. However, SLC39A14 functions as the hepatic transporter of NTBI in the absence of TF [54,55].…”

The Performance of HepG2 and HepaRG Systems through the Glass of Acetaminophen-Induced Toxicity

“…Both cell lines were cultured in a monolayer and treated with increasing concentrations of APAP or 15 mM APAP in the presence or absence of an inhibitor. Caspase 3/7 activity was determined by fluorimetry (Figure 5, top graphs) [65]. We also investigated real-time caspase activation by a fluorescently labeled caspase substrate using fluorescence microscopy (Figure 5, bottom images).…”

The Possible Connection of Two Dual Function Processes: The Relationship of Ferroptosis and the JNK Pathway

“…Cells that overexpress the members of the aldo-keto reductase type 1C family, which have the ability to detoxify the toxic lipid metabolites produced by the oxidative lipid fragmentation during the execution of ferroptosis, showed resistance to the ferroptosis inducer erastin [ 30 ]. The potential role of the lipid alkoxyl radical derivative, acrolein, in plant ferroptosis, such as cell death, has also been shown by our research group [ 31 ]. Thus, it has particular importance that 4-hydroxynonenal is an activator of both the ferroptotic and JNK pathways.…”