Taurine prevents enhancement of acetylcholinesterase activity induced by acute ethanol exposure and decreases the level of markers of oxidative stress in zebrafish brain.

Ethanol (EtOH) is a drug widely consumed throughout the world that promotes several neurochemical disorders. Its deleterious effects are generally associated with modifications in oxidative stress parameters, signaling transduction pathways, and neurotransmitter systems, leading to distinct behavioral changes. Taurine (2-aminoethanesulfonic acid) is a ß-amino acid not incorporated into proteins found in mM range in the central nervous system (CNS). The actions of taurine as an inhibitory neurotransmitter, neuromodulator, and antioxidant make it attractive for studying a potential protective role against EtOH-mediated neurotoxicity. In this study, we investigated whether acute taurine cotreatment or pretreatment (1 h) prevent EtOH-induced changes in acetylcholinesterase (AChE) activity and in oxidative stress parameters in zebrafish brain. The results showed that EtOH exposure (1% in volume) during 1 h increased AChE activity, whereas the cotreatment with 400 mg·L(-1) taurine prevented this enhancement. A similar protective effect of 150 and 400 mg·L(-1) taurine was also observed when the animals were pretreated with this amino acid. Taurine treatments also prevented the alterations promoted in superoxide dismutase and catalase activities by EtOH, suggesting a modulatory role in enzymatic antioxidant defenses. The pretreatment with 150 and 400 mg·L(-1) taurine significantly increased the sulfydryl levels as compared to control and EtOH groups. Moreover, 150 and 400 mg·L(-1) taurine significantly decreased thiobarbituric acid reactive species (TBARS) levels, but the cotreatment with EtOH plus 400 mg·L(-1) taurine did not prevent the EtOH-induced lipoperoxidation. In contrast, the pretreatment with 150 and 400 mg·L(-1) taurine prevented the TBARS increase besides decreased the basal levels of lipid peroxides. Altogether, our data showed for the first time that EtOH induced oxidative stress in adult zebrafish brain and reinforce the idea that this vertebrate is an attractive alternative model to evaluate the beneficial effect of taurine against acute EtOH exposure.

Calcitonin in bone-guided regeneration of mandibles in ovariectomized rats: densitometric, histologic and histomorphometric analysis.

The aim of the present study was to investigate bone promotion in surgical defects created in the mandible of normal and ovariectomized female rats using calcitonin associated with a polytetrafluoroethylene barrier. The 100 female rats were divided into four groups: control (C), control treated with calcitonin (CM), ovariectomized control (OV) and ovariectomized treated with calcitonin (OVM). A circumscribed bone defect 4mm in diameter was created in the region of the mandibular angle, and covered with the barrier. Groups CM and OVM received 2 IU/kg of synthetic salmon calcitonin intramuscularly three times a week. The animals were killed 3, 7, 14, 21 and 28 days after surgery. The bone defects were submitted to densitometric, histologic and histomorphometric analysis. Groups C and CM showed higher levels of bone formation after 7 days compared to the OV and OVM groups. A significant difference was observed between groups C and OV at 3-14 days. The OV group presented slower bone regeneration of the surgical bone defect created in the mandibular angle than group C. Synthetic salmon calcitonin accelerated regeneration of the bone defect in the mandibles of OVM animals similarly to group C, and also increased the formation of new bone during the regeneration process in CM.

Effect of calcitonin on bone regeneration in male rats: a histomorphometric analysis.

The aim of this study was to evaluate the effectiveness of calcitonin in promoting bone growth in surgical bone defects in rat mandibles. Fifty male rats were divided into two groups: bone defect (control) and bone defect with calcitonin (experimental). A circular bone defect 4mm in diameter was made in the mandibular bone of the rats in the angle region, and covered with a polytetrafluoroethylene barrier. The experimental group received 2 IU/kg of synthetic salmon calcitonin intramuscularly three times a week, with treatment starting immediately after surgery. The animals were killed 3, 7, 14, 21 and 28 days after the surgical procedure. The bone defects were examined histologically and by histomorphometric analysis. The Student t-test was applied to the histomorphometric data, with the level of significance set at 5%. The animals of the experimental group showed a lower level of bone formation at almost all time points than the control group, but no difference between groups was observed 28 days after surgery. The volume of newly formed bone matrix was significantly greater in the control than the experimental group at 7, 14 and 21 days, as determined by both morphologic and histomorphometric analysis. Bone repair in the calcitonin-treated animals was delayed in comparison to controls, indicating the need for further studies on male rats.