ABSTRACT
Propolis is a natural product widely used for humans. Due to its complex composition, a number of applications (antimicrobial, antiinflammatory, anesthetic, cytostatic and antioxidant) have been attributed to this substance. Using Saccharomyces cerevisiae as a eukaryotic model we investigated the mechanisms underlying the antioxidant effect of propolis from Guarapari against oxidative stress. Submitting a wild type (BY4741) and antioxidant deficient strains (ctt1∆, sod1∆, gsh1∆, gtt1∆ and gtt2∆) either to 15 mM menadione or to 2 mM hydrogen peroxide during 60 min, we observed that all strains, except the mutant sod1∆, acquired tolerance when previously treated with 25 µg/mL of alcoholic propolis extract. Such a treatment reduced the levels of ROS generation and of lipid peroxidation, after oxidative stress. The increase in Cu/Zn-Sod activity by propolis suggests that the protection might be acting synergistically with Cu/Zn-Sod.
Subject(s)
Antioxidants/pharmacology , Oxidative Stress , Propolis/pharmacology , Saccharomyces cerevisiae/drug effects , Saccharomyces cerevisiae/physiology , Brazil , Drug Tolerance , Hydrogen Peroxide/toxicity , Lipid Peroxidation , Reactive Oxygen Species/analysis , Superoxide Dismutase/analysis , /toxicityABSTRACT
At the concentration used in this work (10 ppm), cadmium was efficiently removed from the environment by stationary yeast cells. While exponential phase cells showed low capacity of cadmium absorption, stationary cells removed 97 percent of the original metal in 24 hours. Total cadmium absorption shown by dry cells was lower than that of fresh ones, although both cells removed 50 percent of metal during the first hour of treatment. We also verified that only viable cells were capable of absorbing cadmium. Independently of the growth phase, cells showed high tolerance to 10 ppm CdSO4 and about 80 percent of cells remained viable after 24 hours exposure to cadmium. However, when stationary phase cells were previously dehydrated and then exposed to cadmium, they exhibited poor survival. By using an oxidation-dependent fluorescent probe, we observed that, once absorbed by cells, cadmium increases the intracellular level of oxidation, which may be responsible for its toxic effect. Crude extracts from stationary phase cells exposed to cadmium showed a 10-fold increase in fluorescence, while extracts from cells of exponential phase did not increase in fluorescence. Dry cells treated with the metal showed a high increase in fluorescence, mainly caused by dehydration.