Caffeic acid treatment alters the extracellular adenine nucleotide hydrolysis in platelets and lymphocytes of adult rats.

This study evaluated the effects of caffeic acid on ectonucleotidase activities such as NTPDase (nucleoside triphosphate diphosphohydrolase), Ecto-NPP (nucleotide pyrophosphatase/phosphodiesterase), 5'-nucleotidase and adenosine deaminase (ADA) in platelets and lymphocytes of rats, as well as in the profile of platelet aggregation. Animals were divided into five groups: I (control); II (oil); III (caffeic acid 10 mg/kg); IV (caffeic acid 50 mg/kg); and V (caffeic acid 100 mg/kg). Animals were treated with caffeic acid diluted in oil for 30 days. In platelets, caffeic acid decreased the ATP hydrolysis and increased ADP hydrolysis in groups III, IV and V when compared to control (P<0.05). The 5'-nucleotidase activity was decreased, while E-NPP and ADA activities were increased in platelets of rats of groups III, IV and V (P<0.05). Caffeic acid reduced significantly the platelet aggregation in the animals of groups III, IV and V in relation to group I (P<0.05). In lymphocytes, the NTPDase and ADA activities were increased in all groups treated with caffeic acid when compared to control (P<0.05). These findings demonstrated that the enzymes were altered in tissues by caffeic acid and this compound decreased the platelet aggregation suggesting that caffeic acid should be considered a potentially therapeutic agent in disorders related to the purinergic system.

Effects of caffeic acid on behavioral parameters and on the activity of acetylcholinesterase in different tissues from adult rats.

Acetylcholinesterase (AChE) is distributed throughout the body in both neuronal and non-neuronal tissues and plays an important role in the regulation of physiological events. Caffeic acid is a phenolic compound that has anti-inflammatory and neuroprotective properties. The aim of this study was to investigate in vitro and in vivo whether caffeic acid alters the AChE activity and behavioral parameters in rats. In the in vitro study, the concentrations of 0, 0.1, 0.5, 1.0, 1.5, and 2mM of caffeic acid were used. For the in vivo study, five groups were evaluated: group I (control); group II (canola oil), group III (10mg/kg of caffeic acid); group IV (50mg/kg of caffeic acid) and group V (100mg/kg of caffeic acid). Caffeic acid was diluted in canola oil and administered for 30 days. In vitro, the caffeic acid increased the AChE activity in the cerebral cortex, cerebellum, hypothalamus, whole blood, and lymphocytes at different concentrations. In muscle, this compound caused an inhibition in the AChE activity at concentrations of 0.5, 1.0, 1.5, and 2mM when compared to the control (P<0.05). In vivo, 50 and 100mg/kg of caffeic acid decreased the AChE activity in the cerebral cortex and striatum and increased the activity of this enzyme in the cerebellum, hippocampus, hypothalamus, pons, lymphocytes, and muscles when compared to the control group (P<0.05). The amount of 100mg/kg of caffeic acid improved the step-down latencies in the inhibitory avoidance. Our results demonstrated that caffeic acid improved memory and interfered with the cholinergic signaling. As a natural and promising compound caffeic acid should be considered potentially therapeutic in disorders that involve the cholinergic system.

Fe(II) and sodium nitroprusside induce oxidative stress: a comparative study of diphenyl diselenide and diphenyl ditelluride with their napthyl analog.

Here, we compare the influence of molecular structural modifications of diphenyl diselenide (DPDS) and diphenyl ditelluride (DPDT) with their naphthalene analogs, 1-dinapthyl diselenide (1-NapSe)2, 2-dinapthyl diselenide (2-NapSe)2, 1-dinapthyl distelluride (1-NapTe)2, and 2-dinapthyl ditelluride (2-NapTe)2. Fe(II)-induced hepatic thiobarbituric acid reactive species (TBARS) was in the order [(2-NapTe)2] > [(2-NapSe)2] > [(DPDS)] > [(1-NapSe)2] > [(1-NapTe)2]> [(DPDT)]. For sodium nitroprusside (SNP)-induced hepatic TBARS, the order was [(2-NapTe)2] > [(DPDT)] > [(1-NapSe)2] > [(2-NapSe)2] > [(1-NapTe)2] > [(DPDS)]. For Fe(II) and SNP-induced renal TBARS, the orders were [(2-NapTe)2] > [(1-NapTe)2] = [(DPDT)] > [(1-NapSe)2] > [(2-NapSe)2] > [(DPDS)] and [(2-NapTe)2] > [(1-NapTe)2] > [(1-NapSe)2] > [(2-NapSe)2] > [(DPDS)] > [(DPDS)], respectively. The present investigation shows that DPDS was less potent and the change in the organic moiety from an aryl to napthyl group dramatically changed the potency of diselenides. These results suggest that minor changes in the organic moiety of aromatic diselenides can profoundly modify their antioxidant properties. In view of the fact that the pharmacological properties of organochalcogens are linked, at least in part, to their antioxidant properties, it becomes important to explore the pharmacological properties of dinaphtyl diselenides and ditellurides.