Propyl gallate promotes salt stress tolerance in green microalga Dunaliella salina by reducing free radical oxidants and enhancing β-carotene production

Abstract

The objective of present work was to study the role of n-propyl gallate (PG), a synthetic antioxidant, in antioxidative responses and salinity tolerance in Dunaliella salina. Algal cultures containing three level of salinity (1, 2 and 3 M NaCl) were treated with two level of 0 and 1 mM of PG for 48 h. 3 M NaCl-grown cells exhibited a minor increase in cell density in comparison to other salt treatments. PG treatment had no effect on cell growth under different salinities. However, the chlorophyll and β-carotene contents significantly increased in PG-incubated cells. Protein concentration clearly reduced in PG-incubated cells grown at 1 and 2 M NaCl compared with those of PG-free, whereas, no significant change influenced by PG was obtained at 3 M NaCl. Ascorbate peroxidase assay showed a minor increase at 3 M NaCl compared with 1 and 2 M NaCl-grown cells. Catalase activity decreased concurrently with salt concentrations, while superoxide dismutase activity pronouncedly increased in response to 2 M NaCl accompanied by a statistically equal increase at 1 and 3 M NaCl. However, the activity of all three enzymes significantly decreased in all PG-incubated algae compared with PG-free ones. Along with increase in total and reduced ascorbate in response to salinity and PG treatments, oxidized ascorbate content was significantly decreased. Hydrogen peroxide and malonyldialdehyde accumulation increased concomitantly with salinity. However, a large decrease in these metabolites occurred in response to PG added into the algal cultures. The results suggest that antioxidant enzymes are not pivotal in improving salinity tolerance and only have short-term adjustment effects to protect against salt stress in D. salina. These data also provide the first direct evidence that PG pretreatment ameliorates salinity stress by electron donation to free radical oxidants, and by inducing β-carotene, chlorophyll, and ascorbic acid biosynthesis, rather than activation of antioxidant enzymes.