The embryonic and postembryonic developmental toxicity of imidazolium-based ionic liquids on Physa acuta.

The embryonic and postembryonic developmental toxicity of imidazolium-based ionic liquids (ILs) to the snail Physa acuta was evaluated in this study. The results of embryonic toxicity tests showed that lower concentrations of 1-octyl-3-methylimidazolium bromide ([C8 mim]Br) (1.5 and 2.1 mg/L) inhibited the hatching rate of snail embryos, and partial snails hatched normally and died, while all of the treated embryos died when the exposure concentration was higher than 4.16 mg/L, at which IL caused the deformation, death, and decay of snail embryos. Statistical analyses revealed obvious differences in the hatching rates between three developmental stages in the 2.1 and 2.94 mg/L groups, indicating that the veliger stage is more sensitive to [C8 mim]Br exposure than the blastula and gastrula stages. Furthermore, the 96 h LC50 values of [C8 mim]Br on the tested snails at three developmental stages (juvenile, subadult, and adult) were 70.83 ± 2.99, 97.59 ± 4.05, and 109.3 ± 2.22 mg/L, respectively, indicating that young snails were more sensitive to [C8 mim]Br toxicity than adults. In addition, the 96 h LC50 values of ILs with different alkyl chain lengths, that is, [C12 mim], [C10 mim], [C8 mim], and [C6 mim], in adult snails were 1.35 ± 0.24, 8.96 ± 5.66, 109.3 ± 4, and 359.6 ± 11.6 mg/L, respectively, suggesting that longer alkyl chains can increase the toxicity of imidazolium ILs on snails.

Combining normobaric hypoxia with short-term resistance training has no additive beneficial effect on muscular performance and body composition.

The aim of this study was to determine the effects of short-term resistance training combined with systemic hypoxia on muscular performance and body composition. Eighteen resistance-untrained men (21.3 ± 2.0 years, 172.7 ± 5.5 cm, 67.3 ± 9.7 kg) were matched and assigned to 2 experimental groups: performing 6 weeks of squat exercise training under normobaric hypoxia (H, FiO2 = 15%) or normoxia (N). In both groups, subjects performed 3 weekly sessions (a total of 18 sessions) of 3 sets of back squat at 10-repetition maximum with 2 minutes of rest between sets. Dynamic, isometric, and isokinetic leg strength and body composition were measured under normoxia before and after resistance training. Squat 1 repetition maximum (1RM) improved significantly (p ≤ 0.05) after resistance training in both H and N groups (88.9 ± 16.9 to 109.4 ± 17.0 kg and 90.0 ± 12.2 to 105.6 ± 13.3 kg, respectively). However, there were no changes in maximal isometric and isokinetic leg strength, lean body mass, and fat mass after the resistance training in both groups. In addition, no significant differences were observed between H and N groups in squat 1RM, maximal isometric and isokinetic leg strength, and body composition. The major findings of this study suggest that short-term resistance training performed under normobaric hypoxia has no additive beneficial effect on muscular performance and body composition. In practical terms, our data suggest that the use of systemic hypoxia during short-term resistance training is not a viable method to further enhance muscular performance and body composition in previously resistance-untrained men.

Acute toxicity and responses of antioxidant systems to 1-methyl-3-octylimidazolium bromide at different developmental stages of goldfish.

Acute toxicity of 1-methyl-3-octylimidazolium bromide ([C(8)mim]Br) to goldfish at different developmental stages and responses of the antioxidant system in adult goldfish were evaluated in the present study. The results indicate that post-embryonic developmental toxicity of [C(8)mim]Br on goldfish is developmental-stage dependent. The juvenile and larva goldfish are more sensitive to [C(8)mim]Br-toxicity than the adult fish. Histological observations in adult goldfish reveal that acute [C(8)mim]Br exposure damages the hepatopancreas, intestines, and kidneys, indicating that these are possible target organs of [C(8)mim]Br toxicity in goldfish. Subsequent biochemical assays in adult goldfish show that [C(8)mim]Br also induces changes in the activities of the superoxide dismutase, catalase, glutathione peroxidase, and glutathione content of fish hepatopancreas. These results suggest that [C(8)mim]Br exposure may induce oxidant stress and lipid peroxidation in hepatopancreas of adult goldfish. In addition, we also find that [C(8)mim]Br causes a remarkable increase in malondialdehyde (MDA) levels in the hepatopancreas of adult goldfish, and thus we think that the MDA level change can be a biomarker of [C(8)mim]Br toxicity in goldfish. The present study indicates that ionic liquids can be a threat to the survival, growth, and development of the fish population once they are accidentally leaked into aquatic ecosystems.

Protective effect of salvianolic acid B on chronic pancreatitis induced by trinitrobenzene sulfonic acid solution in rats.

OBJECTIVES: To investigate the effects of salvianolic acid B (Sal-B) on pancreatic damage in experimental chronic pancreatitis. METHODS: Chronic pancreatitis was induced by infusion of trinitrobenzene sulfonic acid into the pancreatic duct in male Sprague-Dawley rats. From the beginning of 5 weeks, the rats in group 2 were treated with Sal-B by gavage for 8 weeks. Salvianolic acid B was given at a daily dose of 10 mg/kg body weight. At the end of 12 weeks, the levels of serum biochemical indexes were measured on an automatic biochemical analyzer; serum hyaluronic acid and laminin levels were determined by radioimmunoassay; pancreatic tissue malondialdehyde (MDA) was analyzed, and the degree of pancreatic damage was determined. RESULTS: The level of serum biochemical indexes were similar in all groups (P > 0.05 for all). Salvianolic acid B treatment did not obviously reduce hyaluronic acid and laminin concentration in blood (P > 0.05). Salvianolic acid B treatment decreased MDA concentration in pancreatic tissue (P < 0.01). Salvianolic acid B clearly improved pancreatic histological findings and prevented the activation of pancreatic stellate cells. CONCLUSIONS: Sal-B treatment decreased MDA concentration in pancreatic tissue, attenuated morphological pancreatic damage, and prevented the activation of pancreatic stellate cells in experimental chronic pancreatitis.