Two tuber callus lines of Solanum tuberosum L., one lacking detectable lipoxygenase (LOX) activity (LOX-null) and the other possessing activity (LOX-active), were treated with arachidonic acid (AA), an elicitor of the hypersensitive response (HR) and LOX substrate. LOX-active calli exhibited HR cell death and browning within 1 h of treatment, with maximum cell death occurring by 24 h. In contrast, tissue browning was not evident in LOX-null calli and cell viability did not change until 24 h after treatment, when only 10-15% of the cells appeared dead. LOX activity was undetectable in the LOX-null line regardless of treatment or sampling time. LOX-active calli exhibited a nearly linear loss of LOX activity, decreasing to 20% of the control levels by 96 h after arachidonic acid (AA) treatment. Polyphenol oxidase (PPO) activities showed large initial increases in calli from both lines, after which the activities declined to levels near that of the controls. Peroxidase (PER) activity in the LOX-active calli increased to over twice that of control levels within 6 h of treatment, but rapidly declined to 50% of the control values after 24 h. PER activity initially declined slightly in the LOX-null calli but increased to levels near those of the controls by 96 h. These results suggest that LOX, which catalyzes the peroxidation of AA, plays roles in the rapid hypersensitive cell death elicited by AA, while other tissue responses to AA function independently of LOX activity.