Impacts of fire cues on germination of Brassica napus L. seeds with high and low secondary dormancy.

Agricultural burning is used in farm management operations; however, information about the impact of fire cues on the release and/or induction of secondary dormancy in crop seeds is scarce. Seeds from two oilseed rape cultivars were induced for high (HD) or low (LD) secondary dormancy using polyethyleneglycol (PEG) pre-treatment, and their germination after exposure to various fire cues was compared to control PEG pre-treated and non-dormant seeds. Non-dormant seed germination was unaffected by various fire cues. Low doses of aerosol smoke released secondary dormancy in HD seeds, while higher doses increased dormancy of LD seeds. Dilute smoke water also released HD seed secondary dormancy, but concentrated smke water enhanced dormancy in both LD and HD seeds. The concentrated aqueous extracts from charred oilseed rape straw only promoted germination of HD seeds, while dilution inhibited LD seed germination. Heat shock (80 °C, 5 min) released secondary dormancy in HD seeds; however, higher temperatures and/or increased exposure time was associated with seed death. GC-MS analyses of smoke water revealed two butenolides and an array of monoaromatic hydroxybenzene compounds with potential germination inhibitor or promoter activity. The extent of secondary dormancy induction in seeds affects their subsequent responses to fire cues. Both aerosol smoke and smoke water have both germination promoter and inhibitor activity. Lacking any butenolides, aqueous extracts of charred straw contain a potential germination stimulating steroid, i.e. ergosterol. The significance of fire-derived cues on behaviour of oilseed rape seeds in the soil seed bank is discussed.

Atorvastatin reduces the myocardial content of coenzyme Q10 in isoproterenol-induced heart failure in rats.

The present study was aimed to study the effects of different doses of atorvastatin on Co Q10 content in the myocardium tissue in rats. A subcutaneous injection of isoproterenol (5 mg/kg/day) for 10 days was used for the induction of heart failure. Rats were randomly assigned to control, treatment with atorvastatin (5, 10, 20 mg/kg/day) and treatment with atorvastatin plus coenzyme Q10 (10 mg/kg/day). Coenzyme Q10 content of myocardium was measured using HPLC method with UV detector after hemodynamic parameters measurements. The malondialdehyde (MDA) content of the myocardium was evaluated in order to determine coenzyme Q10 antioxidative effect. A high dose of atorvastatin (20 mg/kg/day) was significantly reduced the myocardium content of coenzyme Q10 as compared with isoproterenol treated group (p<0.001). Compared with atorvastatin alone treated animals, co-administration of coenzyme Q10 with atorvastatin was improved the level of coenzyme Q10 in the myocardium (p<0.05, p<0.001). Increasing the dose of atorvastatin also led to increase in MDA content of the myocardium (p<0.01). Serum lipid profile showed no changes in atorvastatin treated groups. The results of this study demonstrate that high doses of atorvastatin reduce coenzyme Q10 content of the myocardium and increase lipid peroxidation in myocardium which is reversed by coenzyme Q10 co-administration.