Effect of Aloe vera preparations on the human bioavailability of vitamins C and E.

There are no literature references describing the effect of consumption of Aloe vera liquid preparations on the absorption of water- or fat-soluble vitamins. There is a very large population worldwide which consume vitamins and many people also consume Aloe. Thus we report the effect of Aloe on the human absorption of vitamins C and E, the most popular vitamin supplements. The plasma bioavailability of vitamins C and E were determined in normal fasting subjects, with eight subjects for vitamin C and ten subjects for vitamin E. In a random crossover design, the subjects consumed either 500 mg of ascorbic acid or 420 mg of vitamin E acetate alone (control), or combined with 2 oz of two different Aloe preparations (a whole leaf extract, or an inner fillet gel). Blood was collected periodically up to 24 h after consumption. Plasma was analyzed for ascorbate and tocopherol by-HPLC with UV detection. There was no significant difference in the areas under the plasma ascorbate-time curves among the groups sincerely due to large differences within the groups. For comparative purposes the control area was 100%. The Aloe Gel area was 304%, and Aloe Whole Leaf 80%. Only Aloe Gel caused a significant increase in plasma ascorbate after 8 and 24 h. For vitamin E, the results for the relative areas were control 100%, Gel 369%, and Leaf (198%). Only the Aloes produced a significant increase in plasma tocopherol after 6 and 8 h. Both Aloes were significantly different from the control after 8 h. Aloe Gel was significantly different from the baseline after 24 h. The Aloes slowed down the absorption of both vitamins with maximum concentrations 2-4 h later than the control. There was no difference between the two types of Aloe. The results indicate that the Aloes improve the absorption of both vitamins C and E. The absorption is slower and the vitamins last longer in the plasma with the Aloes. Aloe is the only known supplement to increase the absorption of both of these vitamins and should be considered as a complement to them.

Cholinergic control of catecholamine release in the eel.

The perifused posterior cardinal vein of the American eel (Anguilla rostrata) releases spontaneously dopamine (DA), norepinephrine (NE), and epinephrine (E). NE and E are secreted by innervated chromaffin cells, while DA is most likely released from a component of the vascular wall. Stimulation with acetylcholine strongly enhances the release of DA and E, and to a lesser degree the release of NE. Nicotine stimulates the release of all three catecholamines. Muscarine reduces the basal release of NE. Muscarine does not prevent nicotinic stimulation of NE and E release, but abolishes the nicotine effect on DA release. The muscarinic antagonist atropine stimulates the release of NE, but not of DA and E. The beta-adrenergic receptor antagonist propranolol suppresses the acetylcholine-stimulated release of NE and E, and reduces the DA response. From these findings, it appears that (1) nicotinic receptors regulate NE and E secretion from the chromaffin cells, (2) muscarinic receptors inhibit basal NE release, and (3) acetylcholine-stimulated release of NE and E requires the interaction with adrenergic receptors. On the other hand, DA release involves both nicotinic and adrenergic receptors, while the reduction of nicotine-stimulated (but not basal) DA release involves muscarinic receptors.

Opioid effects on macrovascular dopamine release.

Both alkaloid opiates and met-enkephalin occur in vertebrate chromaffin cells, where they affect catecholamine (CA) secretion. Since the large blood vessels of the eel and the rat release dopamine (DA) from as yet unidentified source(s), we studied the impact of alkaloid opiates and met-enkephalin on the secretion of DA from three macrovessels of the American eel (Anguilla rostrata) in a perifusion system. Codeine, morphine, and met-enkephalin increased the release of DA from both the ventral aorta and the caudal vein. The antagonist naloxone stimulated DA release from the caudal vein, but had no impact on release from the ventral aorta. Only codeine had a significant effect on DA release from the posterior cardinal vein. These findings show that the DA release from the macrovessels is sensitive to opioid substances, and they suggest that the antagonistic effects between alkaloid opiate and opioid peptide, seen in other systems, are absent in large blood vessels. Furthermore, the "unorthodox" stimulatory effect of naloxone in the caudal vein raises the question of as yet unidentified receptor and/or effector systems.