Consumer attitudes and understanding of cholesterol-lowering claims on food: randomize mock-package experiments with plant sterol and oat fibre claims.

BACKGROUND/OBJECTIVES: Few studies have examined consumer acceptability or comprehension of cholesterol-lowering claims on food labels. Our objective was to assess consumer attitudes and understanding of cholesterol-lowering claims regarding plant sterols (PS) and oat fibre (OF). SUBJECTS/METHODS: We conducted two studies on: (1) PS claims and (2) OF claims. Both studies involved a randomized mock-packaged experiment within an online survey administered to Canadian consumers. In the PS study (n=721), we tested three PS-related claims (disease risk reduction claim, function claim and nutrient content claim) and a 'tastes great' claim (control) on identical margarine containers. Similarly, in the OF study (n=710), we tested three claims related to OF and a 'taste great' claim on identical cereal boxes. In both studies, participants answered the same set of questions on attitudes and understanding of claims after seeing each mock package. RESULTS: All claims that mentioned either PS or OF resulted in more positive attitudes than the taste control claim (P<0.0001), despite all products within each study having the same nutrition profile. How consumers responded to the nutrition claims between the two studies was influenced by contextual factors such as familiarity with the functional food/component and the food product that carried the claim. CONCLUSIONS: Permitted nutrition claims are approved based on physiological evidence and are allowed on any food product as long as it meets the associated nutrient criteria. However, it is difficult to generalize attitudes and understanding of claims when they are so highly dependent on contextual factors.

Nationwide product reformulations to reduce trans fatty acids in Canada: when trans fat goes out, what goes in?

The impact of recent efforts to reduce the content of industrially produced trans fatty acids (TFA) in foods has not been systematically assessed in any country. Concerns exist that food manufacturers/restaurants may replace TFA with saturated fat acids (SFA), rather than cis unsaturated fats, or increase the total fat content. We present findings from a national systematic assessment of grocery and restaurant foods likely to contain TFA in Canada in 2005-2007. Of the total of 221 assessed products, 92 (42%) contained TFA (> or = 5% of fatty acids) on initial assessment. Of an unselected sample assessed more than once, 72% were reformulated during 2005-2007: mean+/-s.d. TFA levels decreased from 26+/-13 to 2+/-4%. Following reformulation, one product had similar TFA+SFA content; all others had decreased TFA+SFA and increased cis unsaturated fat content. The total fat content was generally unaffected. The findings suggest that manufacturers/restaurants generally take advantage of costs and efforts of reformulation to not only reduce TFA but also increase the content of cis unsaturated fats.

Comparative health effects of margarines fortified with plant sterols and stanols on a rat model for hemorrhagic stroke.

There is increased acceptance of fortifying habitual foods with plant sterols and their saturated derivatives, stanols, at levels that are considered safe. These sterols and stanols are recognized as potentially effective dietary components for lowering plasma total and LDL cholesterol. Our previous studies have shown that daily consumption of plant sterols promotes strokes and shortens the life span of stroke-prone spontaneously hypertensive (SHRSP) rats. These studies question the safety of plant sterol additives. The present study was performed to determine whether a large intake of plant stanols would cause nutritional effects similar to those seen with plant sterols in SHRSP rats. Young SHRSP rats (aged 26-29 d) were fed semipurified diets containing commercial margarines fortified with either plant stanols (1.1 g/100 g diet) or plant sterols (1.4 g/100 g diet). A reference group of SHRSP rats was fed a soybean oil diet (0.02 g plant sterols/100 g diet and no plant stanols). Compared to soybean oil, both plant stanol and plant sterol margarines significantly (P < 0.05) reduced the life span of SHRSP rats. At the initial stages of feeding, there was no difference in the survival rates between the two margarine groups, but after approximately 50 d of feeding, the plant stanol group had a slightly, but significantly (P < 0.05), lower survival rate. Blood and tissue (plasma, red blood cells, liver, and kidney) concentrations of plant sterols in the plant sterol margarine group were three to four times higher than the corresponding tissue concentrations of plant stanols in the plant stanol group. The deformability of red blood cells and the platelet count of SHRSP rats fed the plant sterol margarine were significantly (P < 0.05) lower than those of the plant stanol margarine and soybean oil groups at the end of the study. These parameters did not differ between the soybean oil and plant stanol margarine groups. These results suggest that, at the levels tested in the present study, plant stanols provoke hemorrhagic stroke in SHRSP rats to a slightly greater extent than plant sterols. The results also suggest that the mechanism by which plant stanols shorten the life span of SHRSP rats might differ from that of plant sterols.

A randomized trial of two levels of iron supplementation and developmental outcome in low birth weight infants.

OBJECTIVES: To investigate the effect of increased iron intakes on hematologic status and cognition in low birth weight infants. STUDY DESIGN: We randomly assigned 58 infants to receive formula with 13.4 mg iron/L (normal iron) or 20.7 mg iron/L (high iron). At baseline, discharge, and at 3, 6, 9, and 12 months' corrected age, we assessed anthropometry; infections; red blood cell hemoglobin, catalase, glutathione peroxidase, red blood cell fragility (hydrogen peroxide test), and superoxide dismutase values; plasma malondialdehyde, ferritin, iron, transferrin, zinc and copper levels; and diet intake. Griffiths' Development Assessment was done at 3, 6, 9, and 12 months only. RESULTS: No statistical differences (P <.05) were noted for weight, catalase or malondialdehyde levels, red blood cell fragility, or Griffith's Development Assessment. Iron intakes were greater in the high iron group except at 12 months. Hemoglobin (high iron, 123 +/- 9; normal iron, 118 +/- 8) was not different at 3 months (P =.07). Plasma zinc levels (high iron, 70 +/- 14; normal iron, 89 +/- 27) and copper levels (high iron, 115 +/- 26; normal iron, 132 +/- 27; P =.06) at 12 months suggested inhibition of absorption by high iron formula. Glutathione peroxidase levels were higher in the high iron group. The total number of respiratory tract infections was greater in the high iron group (3.3 +/- 0.9) than in the normal iron group (2.5 +/- 0.9). CONCLUSION: In terms of cognitive outcome, there is no advantage associated with elevated iron intake for low birth weight infants.

Superoxide dismutase and glutathione peroxidase content of human milk from mothers of premature and full-term infants during the first 3 months of lactation.

BACKGROUND: Human milk contains various bioactive compounds including numerous immunologic factors, enzymes, growth factors, and hormones. However, the change during the course of lactation in many of these compounds has not been fully characterized. Therefore, the objective of the present study was to measure the activity of the enzymes superoxide dismutase (SOD; Enzyme Commission number [EC] 1.15.1.1) and glutathione peroxidase (SeGSHPx; EC 1.11.1.9) in human milk, to record changes in enzyme activity over time and to determine whether there are differences in activity between the milk of mothers of full-term (FT) and premature (PT) infants. METHODS: Nine samples were collected from each of 15 mothers (32 +/- 4 years of age; mean +/- standard deviation) of FT infants (gestational age, 40 +/- 1 weeks; birth weight, 3544 +/- 417 g) and 19 mothers (28 +/- 5 years of age) of healthy PT infants (gestational age, 29 +/- 4 weeks; birth weight, 1312 +/- 479 g). Samples were collected within a week of birth (+/- 1 day) and thereafter for 8 weeks, with a final collection at 12 weeks. RESULTS: During the 12-week study period, in both groups, total milliunits of GHSPx and SeGHSPx per milligram protein and SOD per per milligram protein increased, whereas protein content declined. SeGHSPx per milliliter milk was higher in the PT group at week 1 (92 +/- 30 mU/mL vs. 73 +/- 21 mU/mL), week 2 (93 +/- 28 mU/mL vs. 75 +/- 24 mU/mL), and week 7 (85 +/- 24 mU/mL vs. 68 +/- 22 mU/mL). The SOD activity per milliliter milk and milligram protein was higher throughout the entire study in the FT milk. CONCLUSIONS: Because mothers of PT infants may produce less milk than those of FT infants, PT infants may be at a disadvantage for antioxidant protection from these enzymes.

Influence of sources of dietary oils on the life span of stroke-prone spontaneously hypertensive rats.

In recent studies, the life span of stroke-prone spontaneously hypertensive (SHRSP) rats was altered by a variety of dietary fats. It was relatively shorter in rats fed canola oil as the sole source of fat. The present study was performed to find out whether the fatty acid profile and the high content of sulfur compounds in canola oil could modulate the life span of SHRSP rats. SHRSP rats (47 d old, n = 23/group) were matched by body weight and systolic blood pressure and fed semipurified diets containing 10% canola oil, high-palmitic canola oil, low-sulfur canola oil, soybean oil, high-oleic safflower oil, a fat blend that mimicked the fatty acid composition of canola oil, or a fat blend high in saturated fatty acids. A 1% sodium chloride solution was used as drinking water to induce hypertension. After consuming the diets for 37 d, five rats from each dietary group were killed for collection of blood and tissue samples for biochemical analysis. The 18 remaining animals from each group were used for determining their life span. The mean survival time of SHRSP rats fed canola oil (87.4+/-4.0 d) was not significantly different (P > 0.05) from those fed low-sulfur canola oil (89.7+/-8.5 d), suggesting that content of sulfur in canola oil has no effect on the life span of SHRSP rats. The SHRSP rats fed the noncanola oil-based diets lived longer (mean survival time difference was 6-13 d, P < 0.05) than those fed canola and low-sulfur canola oils. No marked differences in the survival times were observed among the noncanola oil-based groups. The fatty acid composition of the dietary oils and of red blood cells and liver of SHRSP rats killed after 37 d of treatment showed no relationship with the survival times. These results suggest that the fatty acid profile of vegetable oils plays no important role on the life span of SHRSP rat. However, phytosterols in the dietary oils and in liver and brain were inversely correlated with the mean survival times,indicating that the differential effects of vegetable oils might be ascribed, at least partly, to their different phytosterol contents.

Vegetable oils high in phytosterols make erythrocytes less deformable and shorten the life span of stroke-prone spontaneously hypertensive rats.

Previous studies have shown that canola oil (CA), compared with soybean oil (SO), shortens the life span of stroke-prone spontaneously hypertensive (SHRSP) rats, a widely used model for hemorrhagic stroke. SHRSP rats are highly sensitive to dietary cholesterol manipulations because a deficiency of membrane cholesterol makes their cell membranes weak and fragile. Phytosterols, abundant in CA but not in SO, can inhibit the absorption of cholesterol and also replace a part of cholesterol in cell membranes. This study was performed to determine whether the high concentration of phytosterols in CA might account for its life-shortening effect on SHRSP rats. Male, 35-d-old SHRSP rats (n = 28/group) were fed semipurified diets containing CA, SO, CA fortified with phytosterols (canola oil + phytosterols, CA + P), SO fortified with phytosterols (soybean oil + phytosterols, SO + P), corn oil (CO), olive oil (OO) or a fat blend that mimicked the fat composition of a representative Canadian diet (Canadian fat mimic, CFM; 10 g/100 g diet). These fats provided 97, 36, 207, 201, 114, 27 and 27 mg phytosterols/100 g diet, respectively. Ten rats from each group were killed after 30-32 d for blood and tissue analyses. The remaining rats (18/group) were used for determination of life span. The life span of SHRSP rats fed the high phytosterol oils (CA, CA + P, SO + P and CO) was significantly (P<0.05) shorter than that of CFM- and SO-fed rats. At 30-32 d, the groups fed the high phytosterol oils had greater levels of phytosterols and significantly (P<0.05) higher ratios of phytosterols/cholesterol in plasma, RBC, liver and kidney, and a significantly (P<0.05) lower RBC membrane deformabilty index than the groups fed oils low in phytosterols (SO, OO and CFM). The mean survival times were correlated with RBC deformability index (r(2) = 0.91, P = 0.0033) and cholesterol concentration (r(2) = 0.94, P = 0.0016), and inversely correlated with RBC phytosterol concentration (r(2) = 0.58, P = 0.0798) and phytosterols/cholesterol (r(2) = 0.65, P = 0.0579), except in the OO group. This study suggests that the high concentration of phytosterols in CA and the addition of phytosterols to other fats make the cell membrane more rigid, which might be a factor contributing to the shortened life span of SHRSP rats.

Eighteen-month follow-up of infants fed evaporated milk formula.

In parts of Canada including Newfoundland and Labrador and among Aboriginal peoples, infants still consume evaporated milk (EM) formulas for cultural and economic reasons. At 3 and 6 months, full-term infants fed EM (n = 30) received low intakes of iron, thiamine, selenium and had higher weight velocity than breastfed (BF, n = 29) infants. EM infants had greater anemia, lowered transketolase activity (thiamine) and lowered glutathione peroxidase (selenium) activity (p < 0.05). To determine the later effect of early feeding deficit on nutritional status, we examined these same infants at 18 months of age. At that time, there were no differences in dietary intakes of energy, protein, zinc, copper, selenium and iron, nor in plasma levels of zinc, copper, vitamin C, nor in red blood cell activity levels of glutathione reductase (riboflavin), transketolase, glutathione peroxidase, nor in superoxide dismutase. However, EM infants weighed more and were more likely to visit a physician, have anemia, and have iron depletion than were BF infants. We conclude that infants consuming evaporated milk formulas should receive iron supplements throughout infancy.

Influence of feeding alkaline/heat processed proteins on growth and protein and mineral status of rats.

Effects of feeding alkaline (0.1 N NaOH) and heat treated (75 degrees C for 3 h) proteins (lactalbumin and soybean protein isolate, SPI) on growth, and protein and mineral status of rats have been determined. The untreated and alkaline/heat treated lactalbumin contained 0.10 and 4.42 g lysinoalanine (LAL)/100 g protein, respectively. Similarly, the untreated and treated SPI contained 0.03 and 1.94 g LAL/100 g protein, respectively. The formation of LAL in the treated proteins was accompanied with a loss of cystine (73-77%), threonine (35-45%), serine (18-30%) and lysine (19-20%). The alkaline/heat treatments caused significant (P < 0.05) reductions in protein digestibility of lactalbumin (99 vs. 73%) and SPI (96 vs. 68%). The processing treatments also caused a drastic negative effect on protein quality, as measured by rat growth methods such as relative protein efficiency ratio (RPER) and relative net protein ratio (RNPR). The RPER and RNPR values of untreated lactalbumin and SPI were 89-91 and 56-64%, respectively. But the RPER and RNPR values of the treated lactalbumin and SPI were 0%. The mineral status of rats was also compromised by feeding alkaline/heat treated proteins. Liver iron levels in male rats (165-180 micrograms/g dry weight) and female rats (306-321 micrograms/g dry weight) fed the treated proteins were about half the levels in male rats (229-257 micrograms/g dry weight) and female rats (578-697 micrograms/g dry weight) fed the untreated proteins. The kidney iron contents of rats fed the treated proteins were also lower than that of rats fed the untreated proteins. Liver copper levels of male and female rats fed the treated proteins were up to three fold higher than those found in rats fed the untreated proteins. The data suggested that LAL, an unnatural amino acid derivative formed during processing of foods, may produce adverse effects on growth, protein digestibility, protein quality and mineral bioavailability and utilization. The antinutritional effects of LAL may be more pronounced in sole-source foods such as infant formulas and formulated liquid diets which have been reported to contain significant amounts (up to 2400 ppm of LAL in the protein) of LAL.

Dietary Iodine and selenium interact to affect thyroid hormone metabolism of rats.

The interaction of dietary selenium and iodine on the activities of the selenoenzymes, selenium-dependent glutathione peroxidase (GSH-Px), and type I deiodinase (DI-I), and the thyroid hormones thyroxine (T4) and triiodothyronine (T3) were studied. Male weanling Sprague-Dawley rats were fed an AIN-93G diet for 6 wk with modified selenium and iodine concentration as follows: three levels each of iodine and selenium (0.03, 0.2 added and 1.0 added mg iodine/kg diet, and 0.05, 0.18 added and 1.0 added mg selenium/kg diet) were used in a 3 x 3 factorial design. Renal, but not hepatic, DI-I activity was lower in rats with low selenium intake than in controls. Circulating T3 concentration was not affected by the dietary levels of iodine or selenium. Unlike in liver, kidney and erythrocytes, thyroidal GSH-Px activity was not lower than in controls in rats with low selenium intake, but was significantly higher when iodine intake was low. Significant interactions of iodine and selenium on serum T4 and thyroidal GSH-Px activity were observed. Serum T4 was maintained at control levels when both dietary iodine and selenium were low, but not when iodine alone, or selenium alone, was low. Activity of thyroidal GSH-Px was lowest in rats fed a diet containing high iodine and low selenium. The results suggest that high iodine intake, when selenium is deficient, may permit thyroid tissue damage as a result of low thyroidal GSH-Px activity during thyroid stimulation. A moderately low selenium intake normalized circulating T4 concentration in the presence of iodine deficiency.

Evaluation of full-term infants fed an evaporated milk formula.

The objective of this prospective, cohort study was to compare the nutritional status of full-term infants who were fed human milk (BF, n = 29), formula (FF, n = 30) or evaporated milk formulae (EM, n = 30) for at least 3 months. Infants were seen at enrollment, 3 and 6 months, at which times a blood sample, diet record and anthropometric data were collected. Infants in the EM group received solids earlier (12 +/- 5 weeks) than did FF infants (15 +/- 4 weeks), and both were earlier than BF infants (19 +/- 4 weeks). Only 26% of the EM fed group received iron supplements as ferrous sulphate drops. Seven BF, 12 FF and 20 EM had abnormal ferritin values (< 10 ng ml-1) at 6 months. Copper intake was lower in the EM infants at 3 and 6 months. However, plasma copper and erythrocyte copper zinc superoxide dismutase (ZnCuSOD) levels did not differ between groups. Selenium intake was lower in the EM group (5 +/- 1 and 10 +/- 5 micrograms d-1; 3 and 6 months) than in the FF infants (13 +/- 4 and 19 +/- 7 micrograms d-1; 3 and 6 months). Erythrocyte SeGHSPx levels in EM infants were lower at 6 months (EM, 33.2 +/- 3.4; FF. 35.2 +/- 3.9: BF, 36.1 +/- 3.8 mU mg Hb-1). Thiamin intake (0.99 +/- 0.08 and 1.24 +/- 0.32; 3 and 6 months, mg 1000 kcal-1) was higher in the FF group than in EM infants (0.38 +/- 0.39 and 0.66 +/- 0.38; 3 and 6 months). There were more (13%) abnormal thiamin assays in the EM group at 6 months than in the BF and FF infants (0%). In conclusion, infants fed evaporated milk formula receive adequate copper but may not receive enough thiamin or selenium. Unless supplemented from birth with medicinal iron, intakes of iron will be inadequate.

A method for the determination of type I iodothyronine deiodinase activity in liver and kidney using 125I-labelled reverse triiodothyronine as a substrate.

OBJECTIVES: A detailed method for the determination of iodothyronine deiodinase type 1 (DI-1) activity is described. The objective of the present method development was to consolidate the effective procedures of previous methods and produce an efficient assay that can be easily reproduced. DESIGN AND METHODS: This method uses a 5',-125I labelled rT3 as substrate and ion-exchange chromatography to separate released ionic iodine. Released 125I- collected in the eluate is counted, and the results used to calculate DI-1 activity. RESULTS: Results were found to be linear for tissue homogenates containing 3-11 mg protein.mL-1. Day-to-day coefficient of variation of liver homogenate was determined to be 13%. CONCLUSIONS: This method was found to be reliable, reproducible, and sample sizes as small as 10 microL could be readily assayed. The use of centrifuge filter units to contain the ion-exchange medium decreased handling of the material, and potential sources of error.

Changes in pancreatic glutathione peroxidase and superoxide dismutase activities in the prediabetic diabetes-prone BB rat.

Pancreatic superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) activities were measured during the development of diabetes in diabetes-prone BB rats (BBdp) prior to insulin dependence. The pancreata from seven to eight BBdp rats of each sex were examined at ages 5, 7, 10, and 18 weeks and compared with age-matched control BB rats (BBc). At Week 18, BBdp rats had moderate to high insulitis but normal levels of blood glucose and insulin. Pancreatic CuZnSOD activity in BBdp rats was two times higher than the activity seen in BBc rats at age 5-10 weeks but then declined to the same level as seen in BBc rats at 18 weeks of age. MnSOD activity increased over time in the BBdp rats but remained very low in BBc rats. These changes in CuZnSOD and MnSOD activity resulted in BBdp rats having twice the pancreatic total SOD activity compared with BBc rats (P < 0.0001). Total GSHPx activity was significantly reduced in the pancreata from both male and female BBdp rats compared with their respective controls (P < 0.01 and P < 0.0001, respectively). The lower total GSHPx activity was due to reduced selenium-dependent GSHPx (SeGSHPx) activity. Erythrocyte and plasma activity of these enzymes was not different between rats with or without insulitis, indicating that differences in enzyme activities were confined to the pancreas. Thus, changes in pancreatic antioxidant enzyme activities occur prior to the development of diabetes symptoms in BBdp rats and may be related to the destruction of the pancreatic B cells and ultimate development of diabetes.

Selenium status of very low birth weight infants.

The selenium (Se) intake and status of 82 very low birth weight infants (birth weight 1110 +/- 286 g, gestational age 29.2 +/- 3 wk, mean +/- SD) was assessed at 36.3 +/- 3 postconceptional wk, at 40.1 +/- 4 wk (hospital discharge), and at 3, 6, 9, and 12 +/- 0.75 mo corrected for gestational age. Infants were fed formula containing 0.13 mumol/L (10 micrograms/L) Se. Se-dependent glutathione peroxidase activity in red blood cells declined corresponding to low Se intakes (micrograms/kd/d) for the first 6 mo. With increased consumption of solid foods, intakes of dietary Se and Se-dependent glutathione peroxidase activity increased at 9 mo, suggesting that the earlier supply of Se was suboptimal. Se-dependent glutathione peroxidase activity and intakes of Se were lower in males than in females (p < 0.05). We suggest that infant formulas should probably contain 0.26-0.33 mumol/L (20-25 micrograms/L) Se, particularly those formulas consumed by very low birth weight infants.

Copper status of very low birth weight infants during the first 12 months of infancy.

The Cu intake and status of 106 very low birth weight (VLBW) infants (birth weight 1152 +/- 251 g, gestational age 29 +/- 3 wk, mean +/- SD) were determined approximately 1 mo before hospital discharge, at discharge (time 0), and at 3, 6, 9, and 12 mo +/- 3 wk corrected for gestational age. Infants were fed either formula plus supplemental Zn/Cu (SUPPL, n = 29); formula plus placebo (PLAC, n = 26); or a low birth weight formula (LBWF, n = 26) or were breast-fed (BRMLK, n = 25). Plasma Cu levels in the formula-fed infants increased significantly at each time period with no significant differences between feeding groups. Hair Cu was significantly higher in the SUPPL group compared to the PLAC, LBWF, and BRMLK groups at 3 and 6 mo. Erythrocyte Cu,Zn-superoxide dismutase (CuZnSOD) activity was lowest in the PLAC group. Cu intake was positively correlated with both hair Cu (r = 0.291, p less than 0.0001) and erythrocyte CuZnSOD activity (r = 0.281, p less than 0.001) but not with plasma Cu. An increasing number of formula-fed infants had very low CuZnSOD activity (less than 2 SD below mean) with increasing age (n = 1, 2, 8, 11, and 13 infants at times 0, 3, 6, 9, and 12 mo, respectively). At 12 mo, approximately one third of the formula-fed VLBW infants in this study had low Cu status as assessed by CuZnSOD activity. Infants with the lowest CuZnSOD activity were those with the largest weight gains from 0 to 6 mo and were observed in all formula-fed groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Glutathione peroxidase activity in a healthy Canadian population. Effects of age, smoking and drinking habits, exercise and oral contraceptive use.

The activity of the enzyme glutathione peroxidase (SeGSHPx) has been suggested as an indicator of selenium status. The purpose of this study was to measure the activity of this enzyme in a large sample of healthy, free-living Canadians to determine normal distributions and the effects of age, smoking, and drinking habits, exercise, and the use of oral contraceptives (OCs) or estrogen replacement therapy. The population consisted of 386 self-selected subjects between the ages of 24 and 75. Erythrocyte SeGSHPx activity was 21.5 +or- 7 (Mean +or- SD) and 33.6 +or- 8U/g Hb and plasma activity was 226 +or- 31 and 214 +or- 38 U/L for males (n=239) and females (n=147), respectively. Erythrocyte activity was significantly higher in females and males (p0.01). The Se form of GSHPx accounted for 76% and 54% of total activity in plasma and erythrocytes, respectively. No differences due to age were seen in males, although plasma SeGSHPx, non-SeGSHPx, and total GSHPx activities were elevated in females 65 years of age and older. Cigarette smoking significantly elevated erythrocyte SeGSHPx and total activity in male subjects. This elevation did not vary with the amount smoked and was not seen in ex-smokers. Drinking elevated erythrocyte non-SeGSHPx and total activity in male subjects with the highest activity seen in drinkers who also smoked. No significant differences were seen with level of exercise except for a slight elevation with vigorous exercise. Estrogen use significantly elevated erythrocyte SeGSHPx, non-SeGSHPx, and total activities in both pre- and postmenopausal women. These data suggest that some lifestyle factors can have small but significant effects of GSHPx activity and must be controlled for when population-based surveys are being conducted.

Dietary (n-3) fatty acids affect rat heart, liver and aorta protective enzyme activities and lipid peroxidation.

In a 16-wk study, weanling Wistar rats (32 males and 32 females) were fed a modified AIN-76 diet containing 20% fat with various (n-3) fatty acids. All dietary fats provided the same amount of saturates, monounsaturates, and total essential fatty acids [(n-6) + (n-3)]. The control diet contained lard/corn oil (L/CO). The other diets contained (n-3) fatty acids from linseed oil (LSO), from linseed oil + menhaden oil (LSO + MO) or from menhaden oil (MO). The (n-3) diets reduced total and HDL-cholesterol, particularly in rats fed the MO diet. Platelet thromboxane levels were equally depressed by the LSO and MO diets. Dietary (n-3) fatty acids significantly elevated docosahexaenoic acid in livers and hearts of male and female rats, with females reaching higher levels. This increase was accompanied by reduced arachidonic acid, except for hearts of females in which the major decrease was in linoleic acid. Overall, enzyme activities in the MO-fed group were decreased to the following levels (relative to the activity in the control group): heart Mn superoxide dismutase (SOD), 28%; liver CuZnSOD, 82%; aorta CuZnSOD, 32%. Greater reductions in these enzyme activities were seen in the female rats fed the MO diet compared with male rats. Lipid peroxidation, assessed by urinary, heart and liver thiobarbituric acid reactants, was increased by dietary (n-3) fatty acids (MO greater than LSO + MO greater than LSO greater than L/CO) and was higher in females than in males. These results indicate that enhanced lipid peroxidation occurs with the increased oxidative stress of elevated tissue (n-3) fatty acids accompanied by reduced SOD activity.

Effects of dietary selenium on DMBA-induced carcinogenesis in rats fed a diet high in mixed fats.

The effects of selenium intake on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis were examined in rats fed a diet high in mixed fats and representative of that consumed in North America. Six groups of 20 rats were fed an AIN-76 diet modified to contain 20% fat from lard:corn oil (3:1 wt/wt) and various amounts of selenium (0.1, 0.035, 0.1, 1.0, 2.0 or 4.0 mg Se/kg diet). At wk 5, animals in groups 2-6 were dosed with 4.32 mg of DMBA. Serum clinical parameters and the activities of plasma selenium-dependent and total glutathione peroxidase (GSHPx), erythrocyte GSHPx and superoxide dismutase (SOD) were determined every 4 wk for 25 wk. The extent of lipid peroxidation was determined by measuring urinary malondialdehyde during wk 13 and 24, and erythrocyte malondialdehyde at wk 25. Erythrocyte GSHPx was found to be a better indicator of selenium status than plasma activity, while SOD did not vary with dietary selenium. The group of animals fed 4.0 mg Se/kg diet had reduced numbers of tumors (P less than 0.01), but this reduction was associated with evidence of chronic selenium toxicity. Variations in GSHPx activity with dietary selenium did not result in differences in tumor incidence, nor in changes in lipid peroxidation in the other groups. Thus, nontoxic levels of selenium do not appear to offer any protective effect during carcinogenesis in rats fed a casein-based diet similar in fat content to that consumed by North Americans.