Effect of six months pranayama training on stress-induced salivary cortisol response among adolescents-Randomized controlled study.

BACKGROUND: A combination of yoga practices has been documented to reduce stress and stress-induced cortisol levels. The objective of the current study is to examine the effects of six months of a single pranayama practice (Bhramari [Bhr. P]) on reducing salivary cortisol response to the cold pressor test (CPT) among adolescents. METHODS: Twenty-six healthy adolescents between the ages of 11 and 19 were randomly assigned to either yoga group (n-13) or control group (n-13). Yoga group participants were trained to do Bhr. P for 45 min, thrice a week for six months. All participants underwent CPT at baseline and at end of six months. Saliva samples were collected at baseline (t0), at 20 min (t1), 40 min (t2), and 60 min after the CPT (t3). RESULTS: Contradictory to our hypothesis, participants in the yoga group exhibited a higher salivary cortisol response to the CPT at t1 (p = 0.04) when compared to the control group. However, the t3 salivary cortisol levels showed a statistically significant reduction (p = 0.03) in yoga group when compared to the control group. A significant interaction with time (F (1, 88) = 316.5, p = .001, ηp2:0.91) and between the group × time (F (3, 88) = 2.83, p = 0.04, ηp2:0.8) was found after the intervention. CONCLUSIONS: An increase in the cortisol responsiveness observed in the study is an indication of the adaptive capability achieved through regular yoga training, evidenced by an initial rise in cortisol followed by a rapid fall below baseline after 60 min. Further research is required to conclusively determine the changes in cortisol levels over time in response to stress in long-term yoga practitioners.

Pomegranate Intake Protects Against Genomic Instability Induced by Medical X-rays In Vivo in Mice.

Ionizing radiation (IR) is a well-documented human carcinogen. The increased use of IR in medical procedures has doubled the annual radiation dose and may increase cancer risk. Genomic instability is an intermediate lesion in IR-induced cancer. We examined whether pomegranate extract (PE) suppresses genomic instability induced by x-rays. Mice were treated orally with PE and exposed to an x-ray dose of 2 Gy. PE intake suppressed x-ray-induced DNA double-strand breaks (DSBs) in peripheral blood and chromosomal damage in bone marrow. We hypothesized that PE-mediated protection against x-ray-induced damage may be due to the upregulation of DSB repair and antioxidant enzymes and/or increase in glutathione (GSH) levels. We found that expression of DSB repair genes was not altered (Nbs1 and Rad50) or was reduced (Mre11, DNA-PKcs, Ku80, Rad51, Rad52 and Brca2) in the liver of PE-treated mice. Likewise, mRNA levels of antioxidant enzymes were reduced (Gpx1, Cat, and Sod2) or were not altered (HO-1 and Sod1) as a function of PE treatment. In contrast, PE-treated mice with and without IR exposure displayed higher hepatic GSH concentrations than controls. Thus, ingestion of pomegranate polyphenols is associated with inhibition of x-ray-induced genomic instability and elevated GSH, which may reduce cancer risk.

Comparison of the effects of dietary beef tallow and corn oil on pancreatic carcinogenesis in the hamster model.

We previously reported an enhancement of pancreatic carcinogenesis induced by N-nitrosobis(2-oxopropyl)amine (BOP) in hamsters fed diets containing high levels of corn oil. The research presented here compared diets high in corn oil with those high in beef tallow in the enhancement of pancreatic carcinogenesis. Pancreatic cancer was induced with 20 mg BOP/kg body wt, s.c. administered at 8 weeks of age. One week later, hamsters were assigned to one of five diet treatments: (i) 4.3% corn oil (control); (ii) 20.5% corn oil (high corn oil); (iii) 0.5% corn oil + 3.8% beef tallow (low beef tallow); (iv) 0.6% corn oil + 19.9% beef tallow (high beef tallow); and (v) 5.1% corn oil + 15.4% beef tallow (high fat mixture). These diets were fed until the study ended 84 weeks after BOP treatment. Hamsters were trained through pair feeding to consume the same calorie allotment as the control corn oil group. By the end of the experiment, BOP-treated hamsters that were fed diets containing beef tallow were consistently heavier than those fed corn oil. Survival was longer in hamsters fed the high-beef tallow and high-fat mixture compared with the other diet groups. Tumor data were age adjusted to correct for survival differences. Pancreatic adenoma incidence and multiplicity (no./effective animal) were higher in hamsters fed beef tallow than those fed corn oil diets. Carcinoma in situ multiplicity was elevated in hamsters fed high-fat diets irrespective of the nature of fat fed. Pancreatic adenocarcinoma multiplicity was elevated in hamsters fed the low- or high-beef tallow diets compared with the low- or high-corn oil diets. The mixture of fat resulted in an intermediate yield.

Enhancement of BOP-induced pancreatic carcinogenesis in selenium-fed Syrian golden hamsters under specific dietary conditions.

We measured the effects of dietary selenium (Se) on pancreatic cancer induced in Syrian golden hamsters by N-nitrosobis(2-oxopropyl)amine (BOP). The animals were fed six experimental diets that contained different combinations of the following: 0.1, 2.5, or 5.0 ppm Se from sodium selenite or 2.5 ppm Se from D,L-selenomethionine in either a low (6.0%)- or high (24.4%)-fat diet. Se treatment was begun four weeks before BOP treatment, and the high-fat diet was fed from one week after the last BOP treatment. No evidence for inhibition of pancreatic cancer by Se was observed; in fact, with some experimental conditions, high-Se diets increased the pancreatic carcinoma yield. However, the dietary conditions needed for enhancement differed between the sexes. The male hamsters that received the high-fat diet containing 2.5 ppm Se had more carcinomas than did males given the 0.1 ppm Se level. Carcinoma yields in females did not differ between these diets. Females that received 2.5 ppm Se from D,L-selenomethionine had a greater pancreatic carcinoma yield that did those given 0.1 ppm Se diet. However, carcinoma yields did not differ in males fed these diets. Acinar cell nodule yields were generally reduced in hamsters given the high-Se diets, especially when Se levels in the high-fat diets were compared. Prefeeding 0.1 or 2.5 ppm Se did not influence the elution constants of pancreatic DNA from ductal cells, indicating no effect of Se on the repair of BOP-induced, single-strand breaks in DNA from these cells. Measurements in acinar cells suggested a more rapid repair of single-strand breaks in hamsters prefed 2.5 ppm Se than in those prefed 0.1 ppm Se.

Effects of dietary selenium on bis(2-oxopropyl)nitrosamine-induced carcinogenesis in Syrian golden hamsters.

In studies designed to determine the influence of dietary Se on pancreatic carcinogenesis, Syrian golden hamsters were fed unsupplemented torula yeast diet or diet supplemented with 0.1 or 5.0 ppm Se, from sodium selenite, starting at 4 weeks of age until the termination of the study. In separate groups, hamsters were given the diet supplemented with 0.1 ppm Se until 5 days after carcinogen treatment. Then they were fed either the unsupplemented diet or the diet supplemented with 5.0 ppm Se until the end of the experiment. N-Nitrosobis(2-oxopropyl)amine (BOP; CAS; 60599-38-4) treatment was given as a single sc injection of 20 mg/kg (body wt) at 8 weeks of age, and surviving hamsters were killed 50 weeks later. As a measure of Se status, glutathione peroxidase (GSHPX) activities were determined in plasma, erythrocytes, and liver. Values were elevated in animals fed higher levels of dietary Se. BOP treatment depressed plasma GSHPX at 24 hours and elevated erythrocyte and liver values at 4 weeks. Pancreatic ductular adenoma yields were inhibited with each elevation of dietary Se in female hamsters fed the diets, both before and after BOP administration, and were further inhibited in females that were fed diets containing 0.1 ppm Se before BOP administration and that were changed to the unsupplemented or 5.0-ppm-supplemented diets after BOP was given. Pancreatic ductular adenoma yields were highest in all male groups given diets of 0.1 ppm Se before BOP administration, irrespective of the Se level after BOP was fed. Adenoma yields in males were lowest in hamsters fed unsupplemented diet, both before and after BOP treatment. Pancreatic carcinoma yields were low and not influenced by dietary Se. The incidence of hepatic necrosis was elevated in BOP-treated hamsters fed the unsupplemented diet, and that of biliary cystic adenomas was highest in the group fed 0.1 ppm Se before and after BOP treatment.

Dietary fat and selenium effects on ex vivo prostaglandin production in rat colon, kidney, and blood.

The effects were determined of dietary fat and selenium (Se) levels on prostaglandin (PG) production in rat blood, kidney, and colon mucosa. For 30 weeks, male Wistar-derived MRC rats were prefed diets containing low (6 g/367 kcal) or high (20 g/367 kcal) levels of fat with one of three Se supplements from sodium selenite: 0.0, 0.1, or 2.0 ppm Se. PG production was stopped by adding aspirin immediately following removal of the blood, kidney, and colon samples. Separate samples were allowed to incubate 10 or 60 minutes before blockage of PG production for determination of ex vivo PG production. Prostaglandin E2 (PGE2), thromboxane B2, and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay following separation on silicic acid columns. Basal levels of the three PGs were not influenced by diet. PGE2 production in the colon was highest in the group fed the high-fat diet that contained 2.0 ppm Se at 10 and 60 minutes, but PGE2 production in the blood and kidney were not altered by diet. Thromboxane B2 production in the rats' blood was higher in those prefed high-fat diets, but it was not influenced by dietary Se. Production of 6-keto-PGF1 alpha in the blood and thromboxane B2 and 6-keto-PGF1 alpha production by the kidney and colonic mucosa were not influenced by either dietary fat or Se.

Tolerance of low and high dietary selenium throughout the life span of Syrian hamsters.

In lifetime studies on the effects of dietary selenium (Se) levels, Syrian hamsters were fed diets containing low (unsupplemented torula yeast), adequate (0.1 ppm Se supplemented from sodium selenite), or excessive (5 ppm Se supplemented from sodium selenite) levels of Se. A commercial ration was fed to separate groups. Male and female hamsters were assigned to each diet, and blood samples were collected at 54 and 79 weeks of age for determination of Se status. Body weights of male hamsters were generally highest in those fed unsupplemented diets and lowest in those fed 5 ppm Se supplements. Female weights did not differ between the three semipurified diets. Erythrocyte and plasma glutathione peroxidase and blood Se values increased with the increments in dietary Se at the 54- and 79-week measurements. Survival was approximately 40-45% lower in hamsters fed the commercial ration than in those fed semipurified diets, but was not altered by the Se level in the semipurified diet.

Tolerance of diets deficient or excessive in selenium by Syrian hamsters.

Syrian hamsters were fed torula yeast (TY) diets with 8 selenium (Se) supplement levels (0.0-10.0 ppm Se as sodium selenite) or casein (C) diets with 5 supplement levels (0.0-5.0 ppm Se as sodium selenite) for 25 weeks. Whole blood Se, plasma glutathione peroxidase (GSH-Px) activity and erythrocyte GSH-Px activity were measured after 5, 10, 15 and 25 weeks. At 25 weeks hematology was examined and tissue samples analyzed for Se and evaluated for histopathological lesions. While survival was not influenced by dietary Se, food consumption and body weight gain were altered in animals given TY, as those fed 0.0, 0.05 or 10.0 ppm Se consumed less diet. Weight gains at 25 weeks were highest in animals at the 0.1 ppm Se level and reduced in those given unsupplemented TY or 10.0 ppm Se supplements. Hemoglobin, hematocrit and red blood cell counts were reduced in females fed the lowest and highest Se supplements with TY diets. With both C and TY, whole blood Se rose with increasing dietary Se and in the case of TY, Se was elevated with each feeding increment, except between the 0.05 and 0.1 ppm or the 0.25 and 0.5 ppm levels. Plasma GSH-Px increased with rising Se up to 10 ppm, and erythrocyte GSH-Px activity increased up to 5 ppm Se. Erythrocyte GSH-Px values were higher in animals fed C diets. Histopathological observations were normal at all Se levels. Syrian hamsters tolerated dietary Se from 0.05 to 5.0 ppm Se for 25 weeks of observation without detrimental effects.

Toxic effects of dietary selenium in the Syrian hamster.

Selenium (Se) toxicity and utilization was evaluated in hamsters fed casein- and torula yeast-based diets. 4-week-old hamsters received semipurified diets for 21 days. In experiment I diets were supplemented with either 0.25, 10, 20, 40 or 80 ppm Se as sodium selenite (SS) and in experiment II diets were supplemented with 0.1, 5.0 or 10.0 ppm as SS or selenomethionine (SM). Blood and tissue Se concentrations and glutathione peroxidase (GSH-Px) activity were measured at the termination of the feeding period. In both studies growth rate was depressed and food consumption decreased in hamsters given diets supplemented with 10 ppm or greater SS. Mortality associated with Se toxicity occurred only in females fed the 80 ppm Se-supplemented diet. Whole blood and tissue Se concentrations rose with increasing dietary Se and occurred up to the 80 ppm Se level in blood. Liver, kidney and lung Se concentrations were higher in hamsters fed SM than for those fed SS. Plasma GSH-Px activity was not significantly affected by increasing dietary Se levels, and hamsters fed dietary Se levels above 10 ppm did not have increased erythrocyte GSH-Px activity associated with increased blood Se concentrations. Liver GSH-Px activity was higher in SM-fed hamsters. The results suggest that dietary Se, fed as SS, becomes toxic for Syrian hamsters at levels of 10 ppm and above.