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PubMed2005

Citrate and vitamin E blunt the shock wave-induced free radical surge in an in vitro cell culture model.

Free radical formation plays a major role in shock wave lithotripsy induced renal damage. Moreover, previous studies suggest that free radicals may also promote de novo calcium oxalate crystallization of previously damaged urothelium. Citrate is a known inhibitor of renal stone formation and has also been used as a free radical scavenger. Using an in vitro model with Madin-Darby canine kidney (MDCK) cells, we investigated the influence of two free radical scavengers, citrate and vitamin E, on the prevention of the shock wave-induced free radical surge. Suspensions of MDCK cells were placed in containers for shock wave exposure. Six groups of six containers each were examined: (a) no scavengers 0 shocks, (b) no scavengers 100 shocks, (c) citrate 0 shocks, (d) citrate 100 shocks, (e) vitamin E 0 shocks, (f) vitamin E 100 shocks. An unmodified HM3 was used to deliver 100 shocks at 24 kV. The cell groups that were not shocked acted as the control group and were handled identically, except for the lack of shock wave exposure. After shock wave administration, the containers were emptied and cell suspensions were immediately centrifuged. The supernatant was examined for lactate dehydrogenase (LDH) and 8-isoprostane (8-IP), markers of cellular injury and free radical formation, respectively. Intracellular LDH uniformly increased in all groups exposed to shock wave energy. Similarly, 8-IP increased in all shocked groups. However, the 8-IP increase was significantly reduced when the free radical scavengers were employed. As citrate is a well-known inhibitor of calcium nephrolithiasis, its mechanism of action may be further enhanced, based on its ability to reduce free radical formation, by a protective effect on the urothelium. These data further support the use of citrate based medications during the peri-operative period of shock wave lithotripsy, not only to inhibit stone formation and facilitate fragment passage, but also to reduce the incidence of shock wave induced renal damage. Further studies are warranted to clinically test this hypothesis.

Animals↗

PubMed1991

Vitamin E regulates acetylcholine receptor function of molluscan neurons.

1. Intracellular recordings were made from identified LP11, RBc4, D1 and E4 neurons in perioesophageal ganglionic ring with buccal ganglia of the mollusc Helix pomatia. 2. The modulations of acetylcholine (ACh)-induced current by vitamin E in these neurons were investigated using two-microelectrode intracellular recording and voltage-clamp techniques. 3. ACh receptors function on LP11 and RBc4 neurons was strongly regulated by intracellular calcium ions. For these ACh receptors application of 10(-6) to 10(-4) M vitamin E and calcium influx both induced an enhancement of the ACh-induced chloride current. Application of 10(-5) to 5.10(-5) M arachidonic acid on the same identified LP11 and RBc4 neurons was shown to evoke a decrease of the ACh-induced chloride current. 4. The elevation of calcium levels into D1 and E4 neurons induced a faint decrease of ACh-induced chloride current, but vitamin E and arachidonic acid were ineffective. 5. The calmodulin inhibitor, chloropromazine (6.10(-5) M), strongly inhibited the enhancing effect of calcium influx on ACh-induced chloride current in LP11 and RBc4 neurons, but it had a weak influence on the effect of vitamin E. 6. The effect of vitamin E on surface distribution of functional ACh receptors in LP11 and RBc4 neurons was found. 7. Application of 10(-4) to 10(-6) M vitamin E (DL-alpha-tocopherol) triggered mechanisms, which after a 5 to 45-min period lead to appearance of functional ACh receptors on the parts of neuronal soma, which were further from the axon. 8. Arachidonic acid (vitamin F) evoked a disappearance of functional ACh receptors, which were activated by vitamin E.

Animals↗

PubMed2005

Vitamin E gets an F. Research linking high doses of vitamin E to heart failure is causing new worries about the AREDS vitamins for macular degeneration.

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Contraindications↗

PubMed1998

[Steroid osteoporosis].

The author demonstrates on a group of 292 patients (207 women, 85 men) treated on account of various diseases with corticoids laboratory parameters and bone density and records of bone fractures. The bone metabolism is negatively influenced by the action of corticoids on the vitamin D transformation into its active metabolites; as a result of reduced calcium absorption from the gut the reduced calcium level in blood causes secondary hyperparathyroidism and osteoclastic bone resorption is enhanced. On the other hand, corticoids inhibit new formation of bone by suppressing the proliferation of osteoblasts and by interfering with osteoid formation. One quarter of the patients suffers moreover from osteoporomalacia. Two and a half times as many women have steroid osteoporosis, and bone demineralization is enhanced also by other factors caused by the basic disease (immobilization, hypercalciuria, lactose intolerance). By comprehensive treatment using a combination of Ca + F, vitamin D, exercise, thyrocalcitonin, Osteogenon and recently also the third series of bisphosphonates it proved possible to increase within one year the bone density on average by 4.5% of normal values. The number of fractures declined dramatically.

Adrenal Cortex Hormones↗

PubMed1999

[Essential unsaturated fatty acids].

Linoleic and alpha-linolenic acids are essential unsaturated fatty acids which were referred to as vitamin F much earlier. Their biological significance is to be converted to eicosapolyenoic acids including arachidonic acid which are the precursors of bioactive eicosanoids such as prostaglandins, thromboxanes and leukotrienes. Arachidonic acid is released from phospholipids by the catalysis of phospholipase A2, and then subjected to oxygenation by 5-lipoxygenase for leukotriene production and that by cyclooxygenase for prostaglandin and thromboxane formation. There are two isozymes of cyclooxygenase (COX-1 and COX-2). COX-2 is a product of an immediate early gene and an inducible enzyme, which is considered to play an important role in inflammation. COX-1 is a house-keeping enzyme found in platelets, kidney, stomach and many other tissues. Nonsteroidal anti inflammatory drugs currently used inhibit both COX-1 and COX-2 more or less, and causes gastric erosion and ulceration by inhibiting local production of prostaglandin E2. In view of such important roles of COX-2 in inflammation, inhibitors specific for COX-2 have been developed as anti-inflammatory drugs without stomach injury.

Animals↗

PubMedDate not supplied

The effects of polyunsaturated fatty acids (PUFAs) on the sleep parameters of the rat pups.

In order to verify the hypothesis that at least during perinatal life the amount of active sleep (AS) is dependent on the level of the brain maturation, newborn rats received by an i.p. route for 6 days, a polyunsaturated fatty acid (PUFAs) preparation (Vitamin F) in doses of 1, 10 and 100 mg/day. In comparison with diluent alone injected controls, the PUFAs-injected animals presented a decrease in the AS percentage, decrease which was proportional with the dose. In parallel, it was noted a dose-dependent increase in mortality from 10% for 1 to 90% for 100 mg of PUFAs. We concluded that the PUFAs which greatly stimulate the synaptogenesis, enhance the release of a membrane component with a strong AS inhibiting effect, and, at least during perinatal life, the AS could be modulated by this factors and not by the classical neurotransmitters.

Animals↗

PubMed1994

[Epidemiology of chronic venous insufficiency].

From an epidemiological point of view, at least three different entities of chronic venous insufficiency (CVI) can be defined: heavy legs syndrome is experienced by about half the working people of industrialized countries. It is most frequently linked to varicosis, nevertheless, in one case out of three, no venous incompetence is associated. Female sex, prolonged standing position and overweight are other significant risk factors; varicosis comes with modern civilization. Its prevalence is very low in African and Asian or Australasian aborigen populations although immigrant subjects from these regions have the same risk as the population of their host country. Sedentarity, overweight, tight clothing may provide part of the explanation. But the main factor is probably linked to the low fiber diet in industrialized countries through induced constipation and increased abdominal pressure, or because of the associated low vitamin F intake. Varicosis is rarely seen before adulthood, and its prevalence increases with aging. Sex ratio is unbalanced (F/M estimates: 1.5 to 3.5), that is mainly explained by childbearing and hormonal gactors. A familial factor has also been evidenced, with a relative risk of 2, when one parent has varicosis, and about 3 when both are involved; epidemiological data regarding cutaneous trophic changes in CVI are restricted to leg ulcers: 1% of the general population, and 4 to 5% of people aged 80 and more are afflicted. Leg ulcers are frequently found in the post-thrombotic syndrome, but female sex and varicosis are other significant risk factors. Up to now, epidemiological data are too scarce for a definite demonstration of the natural history of the different subsets of CVI. On the other hand, they clearly show that major medical, social and economical problems are involved.

Adult↗

PubMed1958