Menadiol Diacetate

Cadmium (Cd) has shown toxicity to reduce growth and productivity in different plants. The Present study investigated the efficacy of menadiol diacetate (MD) to reduce Cd stress on growth and yield of summer squash plants. The experiment was performed under saturated Hoagland's nutrient solution (control) while the other group was supplemented with 0.1 mM CdCl₂ (Cd stress). Surface sterilized seeds of summer squash were primed in different concentrations (10, 20 µM) of MD as well as in distilled water for 24 h and sown in the pots. Different morphological and physio-biochemical attributes were determined after 35 d of growth whereas the data for yield attributes was collected after 70 d. Cd concentration was determined in various subcellular compartments i.e., cell walls and cell wall debris, chloroplast, cell membrane and other organelles including vacuoles. The Cd stress decreased photosynthetic pigments, osmoprotectants and ultimately caused reduction in the yield attributes. Further, it increased the secondary metabolites and oxidants (MDA and H₂O₂) in the summer squash tissues. Cd exposure also altered ions accumulation in the summer squash tissues by increasing the root and shoot Ca²⁺ (24-93%) and Fe (4-18%) ions while decreasing the Mg²⁺ (31-39%) ions. The MD-priming, particularly at 10 µM concentration mediated increase in the total phenolics, ascorbic acid, and anthocyanins concentration, and thus enhanced growth and yield attributes of summer squash exposed to Cd toxicity. Further, 10 µM MD-priming facilitated Cd compartmentalization in the subcellular compartments mainly in the cell wall (58%) rather than in the chloroplast (18%), cell membrane (7%) and soluble fractions (18%). In this context, cell wall and vacuole were the key compartments for Cd sequestration. This study highlights MD-priming as a potential strategy to counter Cd toxicity in summer squash plants.

Hydroxyl radicals produced by the iron-mediated Fenton reaction are highly reactive, increase lipid peroxide levels, and damage cell membranes, resulting in ferroptosis, an iron-dependent form of cell death. In recent years, the role of ferroptosis in various pathological conditions has garnered interest. Because it is responsible for oxidative stress-induced organ damage, especially cell death associated with ischemia-reperfusion injury and neurological disorders, the inhibition of ferroptosis may ameliorate organ damage. Through a screen of a unique chemical compound library from Osaka University, we identified several structurally distinct compounds that were highly protective against ferroptosis in vitro. Notably, compound #562, which is a tetrahydroxynaphthalene derivative, exhibited a remarkable ability to fully rescue cells from ferroptosis at low concentrations (0.1 µM). A computational analysis revealed its structural uniqueness and high drug-likeness score, indicating its clinical potential. Along with its enhanced efficacy, this suggests that compound #562 may provide alternative modes of action or improved therapeutic potential for ferroptosis-related diseases.