Lipid peroxidation is an early symptom triggered by aluminum, but not the primary cause of elongation inhibition in pea roots.

Abstract

Pea (Pisum sativum) roots were treated with aluminum in a calcium solution, and lipid peroxidation was investigated histochemically and biochemically, as well as other events caused by aluminum exposure. Histochemical stainings were observed to distribute similarly on the entire surface of the root apex for three events (aluminum accumulation, lipid peroxidation, and callose production), but the loss of plasma membrane integrity (detected by Evans blue uptake) was localized exclusively at the periphery of the cracks on the surface of root apex. The enhancement of four events (aluminum accumulation, lipid peroxidation, callose production, and root elongation inhibition) displayed similar aluminum dose dependencies and occurred by 4 h. The loss of membrane integrity, however, was enhanced at lower aluminum concentrations and after longer aluminum exposure (8 h). The addition of butylated hydroxyanisole (a lipophilic antioxidant) during aluminum treatment completely prevented lipid peroxidation and callose production by 40%, but did not prevent or slow the other events. Thus lipid peroxidation is a relatively early symptom induced by the accumulation of aluminum and appears to cause, in part, callose production, but not the root elongation inhibition; by comparison, the loss of plasma membrane integrity is a relatively late symptom caused by cracks in the root due to the inhibition of root elongation.