Heikki Korpela

Lead and cadmium concentrations in maternal and umbilical cord blood, amniotic fluid, placenta, and amniotic membranes.

The lead and cadmium concentrations in maternal and umbilical cord blood and amniotic fluid were determined in 19 parturient women at delivery. Six placental and amniotic membrane tissue specimens were also investigated. The mean lead concentrations (mean +/- SD) in maternal (40.4 +/- 18.2 ng/ml) and umbilical cord (37.1 +/- 13.5 ng/ml) blood were similar and correlated significantly with each other (r = 0.77, p less than 0.001). The lead concentration in amniotic fluid (59.6 +/- 8.3 ng/ml) was significantly higher than in maternal or umbilical cord blood. Cadmium concentrations in maternal blood (1.1 +/- 0.9 ng/ml) and amniotic fluid (1.0 +/- 0.2 ng/ml) were significantly higher (p less than 0.001) than in umbilical cord blood (0.4 +/- 0.2 ng/ml) and there was no significant correlation among these values. The highest concentrations of cadmium (35.1 +/- 24.2 ng/gm of wet weight) and lead (87.3 +/- 154.2 ng/gm of wet weight) were found in the amniotic membranes. Our results show that lead and cadmium accumulate in amniotic fluid and amniotic membranes and that the distribution of lead and cadmium is different in the human maternal-fetoplacental unit. The fetal exposure to lead is similar and that to cadmium, lower, compared with maternal exposure. The inability of the placenta to totally prevent the fetus from exposure to lead and cadmium suggests that pregnant women should avoid occupations where exposure to these toxic elements is possible.

Serum selenium and glutathione peroxidase and plasma lipid peroxides in uterine ovarian or vulvar cancer and their responses to antioxidants in patients with ovarian cancer

The concentrations of serum selenium and plasma lipid peroxides, and the activity of serum glutathione peroxidase (GSH-Px) were measured before any therapy in patients suffering from uterine, ovarian or vulvar cancer, and in association with 1-day combination cytotoxic chemotherapy of ovarian cancer following 1-week supplementation with selenium (96 micrograms/day), vitamin E (300 mg/day), selenium and vitamin E, or placebo. Patients with gynaecological cancer (N = 44) had lower serum concentration of selenium (1.15 +/- 0.04 S.E. mumol/l; P less than 0.05) and serum activity of GSH-Px (404 +/- 13 units/l, P less than 0.01) than the control subjects (N = 56; 1.25 +/- 0.03 mumol/l and 444 +/- 8 units/l, respectively). In association with cytotoxic chemotherapy selenium alone (P less than 0.05), vitamin E alone (P less than 0.05) and both of them together (P less than 0.001) decreased the plasma concentration of lipid peroxides, and the combination of selenium and vitamin E also increased the activity of serum GSH-Px (P less than 0.01). During placebo, cytotoxic chemotherapy did not affect plasma lipid peroxides but it decreased (P less than 0.001) the activity of GSH-Px. Selenium inhibited this effect. Our data suggest that antioxidative mechanisms of patients with gynaecological cancer may be defective and that treatment with selenium and vitamin E results in changes of biochemical factors related to lipid peroxidation.

Serum selenium concentration, glutathione peroxidase activity and lipid peroxides in a co-twin control study on multiple sclerosis

Serum selenium concentration, glutathione peroxidase activity and lipid peroxides were determined in patients with multiple sclerosis (MS). The series consisted of 13 same-sexed twin pairs derived from the Finnish Twin Cohort of 15,815 pairs. Fourteen subjects had a definite and 1 a probable MS, and their 11 co-twins showed no evidence of central nervous system disease. No statistical differences were observed, but the 3 patients with active progressive MS had a higher mean level of lipid peroxides than the rest of the patients. We suggest that serum lipid peroxidation may be involved in the activity of MS.

Serum selenium, glutathione peroxidase, lipids, and human liver microsomal enzyme activity

This study evaluated selenium status in relation to lipid peroxidation, liver microsomal function, and serum lipids in humans. Serum selenium concentration, glutathione peroxidase (GSH-Px) activity, liver microsomal enzyme activity, assessed by plasma antipyrine clearance (AP-CL) rate, and serum lipids were determined in 23 healthy subjects in a double-blind placebo-controlled trial of selenium supplementation. The low selenium concentration (74.0±14.2 μg/L, mean±SD) is attributable to the low selenium content of the diet. Subjects with the lowest selenium levels (n=11) had reduced serum GSH-Px activity, AP-CL rate, high-density lipoprotein cholesterol (HDL-C), and total cholesterol (T-C) as compared with subjects with higher selenium concentrations (n=12). Low AP-CL rates were associated with low HDL-C: T-C ratios. Selenium supplementation, 96 μg/d for 2 wk, increased serum selenium, GSH-Px activity, and the HDL-C: T-C ratio. The results suggest that a low serum selenium level is associated with a decrease in liver microsomal enzyme activity and serum HDL-C and T-C concentrations. Selenium supplementation in subjects with low serum selenium may favorably influence relations between serum lipoproteins connected with the development of atherosclerotic vascular disease.

Increased myocardial and hepatic iron concentration in pigs with microangiopathy (mulberry heart disease) as a risk factor of oxidative damage.

The role of iron was evaluated in pigs that died suddenly of microangiopathy (mulberry heart disease) characterized by myocardial and endothelial cell damage and capillary microthrombosis. Myocardial iron concentration (mean +/- SD) in pigs with microangiopathy (416 +/- 87 micrograms/g, dry weight) was significantly (p less than 0.001) higher than in pigs with other diseases (294 +/- 93 micrograms/g) and in healthy slaughter pigs (231 +/- 43 micrograms/g). Similarly, hepatic iron concentration in pigs with microangiopathy (1,211 +/- 254 micrograms/g) was significantly (p less than 0.001) higher than in pigs with other diseases (873 +/- 296 micrograms/g) and in healthy slaughter pigs (831 +/- 284 micrograms/g). The results indicate that myocardial and hepatic iron concentration was increased in pigs with microangiopathy. Increased myocardial and hepatic iron concentration might have promoted oxidative stress in selenium-vitamin E-deficient pigs and thus contributed to the development of oxidative damage.

Comparative Effect of Selenate and Selenite on Serum Selenium Concentration and Glutathione Peroxidase Activity in Selenium-Depleted Rats

The biological effect of selenate and selenite was compared in selenium-depleted rats by using both serum selenium concentration and glutathione peroxidase activity as an indicator of body selenium status. A single oral dose of selenium (125 micrograms/kg body weight) as sodium selenate or sodium selenite increased serum selenium concentration and glutathione peroxidase activity significantly (p less than 0.001). The effect of selenate and selenite on serum selenium and glutathione peroxidase activity was similar. Serum selenium concentration correlated positively with serum glutathione peroxidase activity both before (r = 0.815; p less than 0.001) and after (r = 0.800; p less than 0.001) treatment. These results indicate that the biological availability of selenate and selenite is similar.

Effect of ascorbic acid on the bioavailability of sodium selenite in selenium-depleted rats as assessed by serum selenium concentration and glutathione peroxidase activity

The effect of ascorbic acid on the bioavailability of sodium selenite was studied in selenium-depleted rats using serum selenium concentration and glutathione peroxidase activity as indicators of the body selenium status. Two groups of male rats were given a single oral dose of selenium (125 μg/kg body weight) as sodium selenite either with or without oral ascorbic acid (30 mg/kg b.w.). Both serum selenium concentration and glutathione peroxidase activity increased significantly (p<0.001) and more than doubled in both groups after selenite supplementation as compared to initial values. The effect of ascorbic acid supplementation on the bioavailability of selenite as assessed by serum selenium and glutathione peroxidase was insignificant. These results demonstrate that oral ascorbic acid supplementation does not interfere with the bioavailability of selenite in selenium-depleted rats under normal feeding conditions.