Role of the Lutoidic Tonoplast in the Senescence and Degeneration of the Laticifers of Hevea brasiliensis

Abstract

An enzymatic NAD(P)H oxidase activity that generates species of toxic oxygen was located at the level of the lutoidic tonoplast. The partial characterization of this enzyme shows that it is insensible towards classical inhibitors of respiratory chains, and still functions at very low oxygen concentrations. It is greatly activated by physiological concentrations of metallic cations (Fe³⁺ and Cu⁺⁺), and by quinone-like compounds, among which naphtoquinones and ubiquinones may act as physiological activators or electron carriers.

The diverse species of toxic oxygen emitted, lead to the peroxidatic degradation of the unsaturated lipids of the membrane and then to destabilisation and lysis of the organelles, in a way similar to that described for the NAD(P)H induced O₂^- production and consecutive membrane alteration by mammalian microsomes or granulocytes.

Intensive hormonal treatment of bark («over-stimulation» with ethrel, an ethylene generator), or too frequent bark wounding (i.e. over-tapping) increase the O₂^- generating activity, and simultaneously decrease the level of cytosolic scavengers. This leads to lysis of the latex organelles and especially of the lutoids (vacuolysosomes), and to subsequent liberation into the latex of the «coagulating factors» which they normally compartmentalize. It results in latex coagulation within the bark of the stressed trees: the so-called «dry-cuts syndrome».

However, the NAD(P)H oxidase activity remains very low and the scavenging activities (superoxyde-dismutase, catalase, glutathion reductase) and chemical scavengers (e.g. reduced thiols) fully efficient, in the latex from healthy non-stressed Heveas (stable latex).

Computer data analysis allowed us to draw a model describing the biochemical events leading to this type of cell degeneration.