Effect of Transcutaneous Electrical Nerve Stimulation on Parotid Saliva Flow in Patients with Hyposalivation.

CONTEXT: In recent days, we have come across an increase incidence of dry mouth as a side effects of drugs and in order to bring an awareness about a simple non- invasive method to increase the salivary flow, we have used TENS which in many way is beneficial to patients with metabolic disorders. AIMS AND OBJECTIVES: The aim is to assess the effectiveness of transcutaneous electrical nerve stimulation on salivary gland function in patients with hyposalivation. SUBJECTS AND METHODS: The present study included total of 25 subjects with complaint of hyposalivation. Written informed consent was obtained from all the participants. Subjects with pacemakers, autoimmune diseases, pregnancy, and history of salivary gland pathology were excluded from the study. Subjects were asked to refrain from eating, drinking, chewing gum, smoking, and oral hygiene procedures for at least 1 h before the appointment. Unstimulated saliva was collected using modified Carlson Crittenden cup placed over the Stenson's duct bilaterally for 5 min and measured. TENS pads were placed over the parotid region and were activated. The intensity control switch was adjusted for patient's comfort. The intensity was turned up 1 increment at a time at 5 s intervals until the optimal intensity level was reached and stimulated saliva was then collected for 5 min using the modified Carlson Crittenden cup and measured. Any increase in parotid salivary flow (SF) with electrostimulation was considered a positive finding. STATISTICAL ANALYSIS USED: A paired t-test, evaluating mean changes in stimulated versus unstimulated SF rates, was applied to look for statistically significant differences using PASW 18.0 for Windows. An independent sample t-test was performed to note difference between genders. RESULTS: There was significant increase in parotid SF in 19 of 25 patients after transcutaneous electrical nerve stimulation. Males showed more salivary secretion when compared to females. CONCLUSIONS: From the results of the study and within limitations of the study, it can be concluded that TENS was effective in increasing the SF rate in hyposalivatory patients with residual saliva. TENS was less effective in patients who are under xerogenic drugs. Thus, TENS may be an ever-growing armamentarium in the management of salivary gland hypofunction when other therapies have failed or are contraindicated.

Fumonisin B1-induced DNA damage in rat liver and spleen: effects of pretreatment with coenzyme Q10, L-carnitine, alpha-tocopherol and selenium.

Active oxygen radical species are reported to cause organ damage. This study was designed to determine whether oxidative stress contributed to the initiation or progression of hepatic and splenic cell DNA damage induced by fumonisin B1 (FB1) in rats. Another aim was to investigate the protective effects of the antioxidants coenzyme Q10 (CoQ10), L-carnitine, vitamin E (alpha-tocopherol) and selenium against DNA damage in the liver and spleen of rats treated with FB1. Fasted rats were injected intravenously with a single dose of fumonisin B1 at 1.55 mg kg-1 body wt. into the tail vein. Treatment with FB1 led to splenic and hepatic DNA fragmentation in 85% of the test animals. DNA fragmentation was investigated as a critical event in toxic cell death by testing total Ca2+ in liver. FB1 administration caused total Ca2+ in liver to increase within 4 h (204% of control). Measurement of liver enzyme activities showed an increase in aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT). FB1 also markedly decreased splenic and hepatic glutathione (GSH) levels. Pretreatment with CoQ10 (30 mg CoQ10 kg-1 diet) together with L-carnitine (2.8 mg carnitine kg-1 diet), alpha-tocopherol (30 IU vitamin E kg-1 diet) and selenium (1 mg selenium as sodium selenite kg-1 diet), decreased DNA damage and the activities of Ca2+, ASAT and ALAT in the liver. On the other hand, the level of GSH was slightly increased. The CoQ10 alone did not significantly protect against toxic cell death and glutathione depletion caused by FB1. Oxidative damage caused by FB1 may be one of the underlining mechanisms of FB1-induced cell injury and DNA damage.

Effect of selenium fertilization on selenium in feedstuffs and selenium, vitamin E, and beta-carotene concentrations in blood of cattle.

Selenium (n = 56), total vitamin E, and homologues of natural vitamin E in feedstuffs (n = 52) and the concentrations of Se (n = 241), vitamin E (n = 244), and beta-carotene (n = 227) in blood were measured. The mean (+/- SD) Se content in hay, grass silage, oats, and barley produced using fertilizers enriched with Se was 0.13 (+/- 0.169), 0.17 (+/- 0.704), 0.23 (+/- 0.107) and 0.21 (+/- 0.119) mg/kg of DM, respectively, and the mean (+/- SD) vitamin E contents, calculated as dl-alpha-tocopherol acetate equivalents, were 39.7 (+/- 13.0), 120.0 (+/- 40.27), 24.4 (+/- 3.83) and 34.5 (+/- 3.57) IU/kg of DM, respectively. The mean Se concentrations in whole blood of cows, heifers, bulls and calves fed hay (n = 62), silage (n = 111), or pasture (n = 68) varied from 183 to 244 micrograms/l. The mean concentrations of total vitamin E in serum of lactating cows fed hay (n = 21), silage (n = 29) or pasture (n = 26) were 2.8 (+/- 1.43), 6.5 (+/- 3.03) and 8.2 (+/- 2.64) mg/l, respectively. For calves, concentrations of vitamin E in serum were as low as 0.25 mg/L. The mean concentration of beta-carotene in serum of lactating cows fed grass silage (n = 26) or pasture (n = 28) was 13.7 (+/- 6.61) and 15.4 (+/- 6.15) mg/L, respectively, but, in lactating cows fed hay (n = 20), concentrations were 2.5 (+/- 1.07) mg/L.

Blood selenium, vitamin E, vitamin A, and beta-carotene concentrations and udder health, fertility treatments, and fertility.

We investigated the activity of glutathione peroxidase in whole blood; concentrations of vitamin E, vitamin A, and beta-carotene in serum; SCC; udder bacterial infections and the incidence of clinical mastitis; fertility treatments; and the success of first AI of 511 dairy cows for 1 yr. The mean Se content in whole blood and the concentrations of vitamin E, vitamin A, and beta-carotene concentrations in serum were 191 micrograms/L, 5.9 mg/L, 0.39 mg/L, and 12.9 mg/L, respectively. An increase in Se concentration in whole blood was associated with a decrease in all infections, including infections by Staphylococcus aureus, Actinomyces pyogenes, and Corynebacterium spp. (-17.7, -31.7, and -70.6%, respectively). There was no association among the different infections or SCC and concentrations of vitamin E, vitamin A, or beta-carotene, but an association existed between vitamin A concentration and SCC. The lower Se concentration in whole blood did not increase incidence of clinical mastitis. The Se concentration in whole blood (200 micrograms/L) was accepted as a target value to optimize udder health. The incidence of fertility disorders (anestrus, subestrus, cystic ovaries, or delayed ovulation) was 34.4%. The pregnancy rate following first insemination was 48.6%. No significant association was observed among Se in whole blood; concentrations of total vitamin E, vitamin A, or beta-carotene in serum; and fertility disorders or success of first AI.

Comparisons of selenite and selenium yeast feed supplements on Se-incorporation, mastitis and leucocyte function in Se-deficient dairy cows.

The dairy cows at the Estonian Agricultural University appeared to have an extremely low selenium status. The selenium level was 5.6 micrograms/l in whole blood and 3.2 micrograms/l in milk, on average. The blood glutathione peroxidase was consequently extremely low. The effects of organic selenium (selenized yeast) and sodium selenite were compared in a feeding experiment on 100 dairy cows. Selenium incorporation, udder health and the in vitro function of blood neutrophils were monitored. Supplementation of the feed either with 0.2 ppm organic selenium or sodium selenite for 8 weeks, increased the blood selenium level (geometric mean) within this period from the back-ground level (about 5.6 micrograms/l) to 167 (Se-yeast) and to 91 micrograms/l (selenite). The respective change in whole blood glutathione peroxidase (GSH-PX) was from 0.22 to 3.0 (Se-yeast) and to 2.3 (selenite) microKat/g Hb. Blood GSH-PX continued to increase up to 10 weeks after the supplementation was stopped. The bioavailability of yeast selenium was superior to selenite: the relative bioavailability (selenite = 1) of yeast selenium was 1.4 if blood GSH-PX, 1.9 if blood selenium, and 2.7 if milk selenium was used as the response criterion. Selenium-supplementation showed a positive effect on udder health. The percentage of quarters harbouring mastitis pathogens dropped from 22.9 to 13.0 in the Se-yeast group and from 18.4 to 7.4 in the selenite group during the supplementation period. The effect of selenium on mastitis was also reflected as a decrease in the output of milk somatic cells and N-acetyl-beta-D-glucosaminidase (NAGase). The time-luminescence profile of zymosan-induced activity of blood neutrophils became skewed to the left in Se-supplemented cows.

Protective effect of antioxidants against free radical-mediated lipid peroxidation induced by DON or T-2 toxin.

An experiment was conducted on rats to investigate the capacity of antioxidants to protect against acute toxicity caused by DON or T-2 toxin. Male rats were fed two different feeds. One group received a feed deficient in vitamins C and E and selenium, whereas the other group was fed with a feed enriched in antioxidants. After two weeks, selected groups of rats were administered orally a single dose of DON or T-2 toxin. After the treatment with mycotoxins, all rats were decapitated. The livers were analyzed for TBARS values, hepatic GSH content and for the activities of CyP-450, CAT, SOD and GSH-TR. Increases in lipid peroxides of 21% and 268% were observed in those rats which did not receive the supplement of antioxidants and which were administered DON or T-2 toxin, respectively. There was no significant increases in the TBARS values in the groups receiving DON with selenium and vitamins, but increases of 57% and 79% were recorded in the groups administered T-2 toxin and antioxidants. Furthermore, in the groups fed the deficient feed and administered DON or T-2 toxin, the lipid peroxidation increased by 33% and 307%, respectively. No mortality, and a lower number of intoxicated animals were observed in rats fed a diet supplemented with antioxidants. Significant decreases of GSH, CAT, SOD, CyP-450 and GSH-TR were recorded in treated rats receiving the deficient feed. The results of this study demonstrate that trichothecenes stimulate lipid peroxidation with consequent decrease of GSH content, but that the dietary use of selenium, alpha-tocopherol and ascorbic acid provides protection against acute toxicosis caused by DON or T-2 toxin.

Utilization of dietary sodium selenite, barley, oats and meat meal selenium by the chick.

The biological availability of selenium (Se) in barley, oats and meat meal as compared to that in sodium selenite was determined by whole blood glutathione peroxidase (GSH-Px) activity and Se concentration depletion-repletion bioassays. One day old White Leghorn chicks, initially of low-Se status, were further depleted for Se by feeding a low-Se casein basal diet (0.03 mg Se/kg diet) adequate in vitamin E for the first two weeks of life. Repletion treatments of Se at graded levels supplemented by the natural sources or sodium selenite were then provided for 4 weeks. A multiple regression equation was calculated to relate the final whole blood GSH-Px activity and Se concentration to the dietary intake of Se. The percent biological availability of Se present in the natural sources was evaluated by slope ratio analyses in comparison to the standard, sodium selenite (100%). The activity of whole blood GSH-Px established a relative bioavailability for barley, oats and meat meal Se of 85, 41 and 25%, respectively (as mu kat/l), and 81, 51 and 17%, respectively (as mu kat/g Hb). The estimated bioavailability of Se in the different natural sources, as measured by blood Se concentration was: barley, 104%; oats, 99% and meat meal, 69% in comparison to that of sodium selenite. Thus, selenite Se was superior to the natural Se sources for the induction of GSH-Px activity. Barley Se appeared to be of higher biological value to chicks than did oats and meat meal Se. Even though meal Se was retained in appreciable amounts in chick blood, it showed the poorest utilization for the synthesis of blood GSH-Px.

Effect of Se status on some haematological parameters in neonatal piglets.

Blood samples were taken from 74 1-3 day old piglets, the offspring of sows maintained during pregnancy on a commercial ration with 0.1 ppm of added Se as sodium selenite. At the time of blood sampling, all piglets were treated subcutaneously with 200 mg Fe+3 from iron dextran. Additional blood samples were taken 14 days after the iron treatment. Piglets with 14 day whole blood Se concentrations greater than 74.0 micrograms/l (n = 43) had significantly higher mean numbers of red blood cells than those with whole blood Se less than or equal to 74.0 micrograms/l (p = 0.016). The mean increase in erythrocyte numbers during the 14 day period was significantly higher in the higher than in the lower Se group (p = 0.007) as also in the piglets with plasma GSH-Px activity greater than 799 U/l at 1-3 days of age when compared to the piglets with the GSH-Px activity less than or equal to 799 U/l (p = 0.017).

Milk and blood levels of silicon and selenium status in bovine mastitis.

Milk and blood levels of silicon, selenium and the selenoenzyme glutathione peroxidase (GSH-Px) were measured in 20 healthy and 21 mastitic cows. In milk samples from healthy quarters the mean silicon concentration was 0.81 and in affected ones 0.39 ppm. In serum the mean silicon values were 1.63 and 1.02 ppm respectively. The selenium status was not altered but the level of erythrocyte GSH-Px was lowered in mastitic animals. Silicon is known to have marked effects on free radical formation, lipid peroxidation and macrophage activity. Its possible role in infection and inflammation is evaluated. Some of the functions of silicon may resemble those of selenium. The possibility of lowered levels of silicon and of the selenoenzyme in mastitis calls for experimentation with dietary or pharmaceutical supplementation of these trace elements.

Possible roles of vitamin E and glutathione metabolism in bovine mastitis.

Plasma and milk levels of vitamin E were determined in mastitic and healthy cows and compared with erythrocyte GSH and GSH-peroxidase, selenium, silicon, prostaglandins and parameters commonly used for diagnosing mastitis. In mastitis both the plasma and milk levels of vitamin E were significantly lowered. In the milk vitamin E correlated negatively with electrical conductivity and PGE2. In the blood vitamin E was in a positive correlation with erythrocyte GSH. The role of lipid peroxidation in relation to the inflammatory and immunological reactions of mastitis is discussed.