Some Effects of Ammonia on Plant Metabolism and a Possible Mechanism for Ammonia Toxicity

Abstract

The mechanism of ammonia toxicity to plants was investigated. O2 uptake in a Warburg respirometer was used as an indication of the effect of gaseous ammonia and ammonium salts on respiration of excised barley roots, garden beet root disks, as well as leaf disks of spinach and sugar beets, and garden beet root mitochondria. Gaseous NH3 and undissociated ammonia in equal concentrations were found to inhibit respiration to the same degree in the tissue studied. The pH level was important in ammonia toxicity to the extent that it controlled the undissociated ammonia concentration. Therefore the undissociated ammonia probably is the effective form of ammonia causing inhibition of respiration in plants. Added substrates were ineffective in overcoming the respiratory inhibition of infiltrated intact tissue or mitochondrial preparations. Substrates studied include glucose, pyruvate, citrate, alpha-ketoglutarate, succinate and malate. Of these only succinate appeared resistant to ammonia. The partial resistance of succinate oxidation to ammonia treatment indicated a possible association with the electron transport system, since succinate does not require diphosphopyridine nucleotide (DPN) as a cofactor. Studies with DPN reduction and oxidation in a recording spectrophotometer at 340 mu showed that the oxidation of reduced diphosphopyridine nucleotide (DPNH) was inhibited by ammonia treatment. The companion reaction, DPN reduction, was speeded up following ammonia treatment, probably due to the competition of the 2 simultaneous reactions. It is suggested that the site of ammonia toxicity to plants is located in the electron transport system, specifically on the DPNH [forward arrow] DPN reaction.