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Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 wk. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 or 8 wk. The control groups comprised rats not injected with STZ and fed either Mn-deficient or Mn-sufficient diets for a total of 12 wk. The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in the non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Plasma and hepatic vitamin E levels increased progressively with the duration of diabetes, independent of dietary Mn intake. Lipid peroxidation, as measured by H2O2-induced production of thiobarbituric acid reactive substances in erythrocytes, also increased, concomitant with decreased liver and kidney glutathione (GSH) levels. These findings demonstrate for the first time and interactive effective between Mn deficiency and STZ-diabetes, resulting in amplification of tissue antioxidant changes seen with either Mn deficiency or STZ-diabetes alone. This effect of Mn deprivation in experimental diabetes suggests a physiological role for Mn as an antioxidant nutrient.

To investigate the placental enlargement which accompanies maternal alcohol consumption during pregnancy, Sprague-Dawley rats were given 20% ethanol for 4 weeks prior to mating and 30% ethanol throughout gestation. Pair-fed controls received an isocaloric amount of corn starch and chow, with water ad libitum, and ad libitum controls received rat chow and water. On days 17, 18, 19 and 20 of gestation, placentas were removed for histological observation. On days 18–20, the placentas of alcohol-fed rats weighed significantly more than did those of controls, although there was no difference in weight on day 17. Giant cells in the basal zone were significantly increased in number and size in alcohol-fed rats compared to controls. Trophoblastic cells in the basal zone were significantly larger in the alcohol group than in the control groups except on day 17. The maternal blood channels in the labyrinth were wider and more filled with blood corpuscles in the alcohol group than in either control group. It is concluded that the increased weight of the placenta may be largely due to the stagnated maternal blood cells in the labyrinthine blood channels and also to the increased number and size of giant cells and the enlarged trophoblastic cells in the basal zone.