Fresh fruit and vegetables are highly perishable because of their active metabolism during the postharvest phase. Previous studies showed that hormic dose of UV cause a delay in the senescence of tomato fruit by about 7 days. The objective of this study was to elucidate whether UV acts on the cell membrane in producing the phenomenon of delayed senescence, since it is known that UV radiation can provoke photooxidation of membrane lipids. Membrane lipid peroxidation was studied in tomato fruit (Lycopersicon esculentum Mill cv. Trust) treated by hormic UV dose, and was followed by assaying products of lipid oxidation during the storage period. We observed the production of lipofuscin-like compounds, malondialdehyde, aldehydes, pentane, ethane, and hydrogen peroxide within few days of the treatment. An increase in the efflux of electrolytes (total, potassium, and calcium) was also observed. An immediate increase in the level of these products of oxidation supports the hypothesis that UV radiation induces membrane lipid peroxidation. However, beyond 5 to 7 days after treatment, the production of oxidation products and electrolyte leakage were lower than the control fruits. Thereafter, the level of products of lipid oxidation associated with senescence was higher in control fruits than in treated ones. Results suggest that the initial oxidation stress by the exposure to UV led to biochemical reactions inducing the production of stress compounds, such as polyamines, which are non specific antioxidants. Consequently, a delay in the senescence was observed.