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Biomedical subjects

R A Lawrence

Publications and source records attributed to R A Lawrence.

At least 127 records · Page 7Linked to original sources
PubMed1982

Effects of copper deficiency on the activity of the selenoenzyme glutathione peroxidase and on excretion and tissue retention of 75SeO3(2-).

Liver and lung activities of the antioxidant enzymes glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were determined in control and copper-deficient rats. Decreased activity of SOD was found in liver and decreased activity of the selenoenzyme GSH-Px was found in liver and lung in the copper-deficient animals. The decreased liver activity of GSH-Px could be partially corrected by daily supplementation of the basal diet with sodium selenite. Urinary, fecal and biliary excretion of 75SeO3(2-) were determined in controls and copper-deficient rats in order to assess selenium losses. Urinary excretion of 75Se was not different in the two groups. Fecal loss of 75Se was increased in the copper-deficient animals when compared to controls and biliary excretion was decreased. Tissue retention of 75Se was also determined in both groups. Retention of 75Se in the copper-deficient rats was increased in brain and lung and decreased in liver. This pattern of tissue retention of 75Se is similar to that which occurs in selenium-deficient rats. Copper deficiency in rats results in decreased liver activity of both the copper-containing enzyme SOD and the selenoenzyme GSH-Px. The mechanism of decreased GSH-Px activity is unknown.

Animals↗
PubMed1982

Inability of niacin to protect from in vivo hyperoxia or in vitro microsomal lipid peroxidation.

The efficacy of niacin in protecting rats from normobaric hyperoxia was evaluated in vivo by exposing niacin treated animals and controls to greater than 95% O2 for 96 hours. The vitamin was also evaluated as a possible free radical scavenger in vitro using an Fe-ascorbate initiated microsomal lipid peroxidation system. No protective effects were observed in vivo either in mortality or in differences in lung wet and dry weights of the niacin treated rats when compared to controls. Niacin in varying concentrations also did not decrease lipid peroxidation in the microsomal systems. Although this vitamin has been reported to protect animals from paraquat toxicity when given intraperitoneally once daily, niacin administered in similar doses does not appear to protect rats from hyperoxia.

Animals↗
PubMed1982

Practices and attitudes toward breast-feeding among medical professionals.

The results of a mail survey conducted among pediatricians, obstetricians, family practitioners, and nurses, and results of an adjunct survey conducted among hospital administrators are presented. According to the findings, breast-feeding is advocated by physicians; however, the topic is not always initiated, so the mother is influenced by other sources. Supplementary foods and vitamins are advocated to varying degrees and not necessarily in keeping with present knowledge about nutrition. Physicians are willing to counsel mothers regarding problems with breast-feeding and feel that further physician encouragement is necessary for more breast-feeding or longer breast-feeding. Mothers should have an opportunity during pregnancy, while they are in the hospital, and postnatally to learn as much as they can about feeding methods. The obstetrician can initiate earlier discussion with the mother on feeding methods and can assume a more aggressive role in initiating this discussion. In the hospital, a mother who chooses to breast-feed can be assisted in having a successful breast-feeding experience by spending as much time as possible with her infant starting with the period immediately following birth. Postnatally, physicians can encourage successful breast-feeding and breast-feeding of longer duration by not encouraging the early initiation of supplements and solid foods. The increasing trend in breast-feeding can best be facilitated by these positive actions taken by physicians, nurses, and health care facilities.

Adult↗
PubMed1981

Discrimination of the age of adolescent females on the basis of facial cues.

In an ongoing study of adolescent maternal-infant interaction, we investigated the accuracy with which judges could assign the age of two groups of females, based on videotaped facial cues alone. The two groups were eight "adolescents," whose ages were less than or equal to 17 years, and 20 "adults," whose ages were greater than 20 years. Twenty-seven judges, whose average age was 28.7 years with a range from 27 through 44 years of age, were asked to judge the ages of the subjects in the two groups. Overall, the judges were successful in identifying adolescents 41.8% of the time. There was no relationship between the ages of the judges and the accuracy of their judgments. On the basis of facial cues alone, our results clearly suggest that the process of assigning an individual to an adolescent or adult group is essentially random, approaching a 50/50 breakdown. This study supports the concept that observed differences between adolescents and adults interacting with their infants is due to actual differences in behavior and not the cultural bias of the judge.

Adolescent↗
PubMed1981

Hepatic cytochrome P-450 and microsomal heme oxygenase in copper-deficient rats.

Copper deficient and control rats were pair-fed from weaning a milk-based diet. Each animal received 25 mg of iron parenterally. After 6 weeks of dietary manipulations the animals were killed. As expected, rats fed the copper-deficient diet were anemic. Copper-dependent enzyme activities and copper content of plasma and liver confirmed that copper deficiency was present in these rats. Hepatic microsomal cytochrome P-450 specific contents were similar in control and copper-deficient animals in the uninduced state and following induction of cytochrome P-450 by treatment with phenobarbital. However, microsomal heme oxygenase was increased in copper-deficient animals compared with controls whether they were treated with phenobarbital or not. No differences were observed in splenic microsomal heme oxygenase between dietary groups. These studies suggest that hepatic heme catabolism is enhanced in copper deficiency. The explanation for this enhancement may be related to increased hepatic iron accumulation in copper-deficient animals or to the associated defect of selenium metabolism in copper deficiency.

Animals↗
PubMed1980

Rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system.

Dialyzed rat liver cytosol (105 000 X g supernatant), when added along with 2.5 mM glutathione, blocked malonaldehyde formation in the NADPH-microsomal lipid peroxidation system, thus protecting against lipid peroxidation. Preheating the cytosol for 10 min at 60 degrees C destroyed its protective ability. Ammonium sulfate fractionation and Sephadex G-100 gel filtration of cytosol indicated that more than one glutathione-dependent protective enzyme was present. Fractions from the G-100 column containing the selenoenzyme glutathione peroxidase failed to protect, but fractions containing the glutathione S-transferases, which have non selenium-dependent glutathione peroxidase activity, did protect. The glutathione S-transferases were purified further with ion exchange chromatography and shown to have protective activity. Thus the rat hepatic cytosolic glutathione-dependent enzyme protection against lipid peroxidation in the NADPH-microsomal lipid peroxidation system is in part due to some of the glutathione S-transferases. The selenium-dependent glutathione peroxidase appears to have no protective effect in this system.

Animals↗
PubMed1980

Liver necrosis and lipid peroxidation in the rat as the result of paraquat and diquat administration. Effect of selenium deficiency.

Paraquat and diquat facilitate formation of superoxide anion in biological systems, and lipid peroxidation has been postulated to be their mechanism of toxicity. Paraquat has been shown to be more toxic to selenium-deficient mice than to controls, presumably as the result of decreased activity of the selenoenzyme glutathione peroxidase. The present study was designed to measure lipid peroxidation and to assess toxicity in control and selenium-deficient rats given paraquat and diquat. Lipid peroxidation was measured by determining ethane production rates of intact animals; toxicity was assessed by survival and by histological and serum enzyme evidence of liver and kidney necrosis. Paraquat and diquat were both much more toxic to selenium-deficient rats than to control rats. Diquat (19.5 mumol/kg) caused rapid and massive liver and kidney necrosis and very high ethane production rates in selenium-deficient rats. The effect of paraquat (78 mumol/kg) was similar to that of diquat but was not as severe. Acutely lethal doses of paraquat (390 mumol/kg) and diquat (230 mumol/kg) in control rats caused very little ethane production and no evidence of liver necrosis. These findings suggest that paraquat and diquat exert their acute toxicity largely through lipid peroxidation in selenium-deficient rats. Selenium deficiency had no effect on superoxide dismutase activity in erythrocytes or in 105,000 g supernate of liver or kidney. Glutathione peroxidase, which represents the only well-characterized biochemical function of selenium in animals, was dissociated from the protective effect of selenium against diquat-induced lipid peroxidation and toxicity by a time-course study in which selenium-deficient rats were injected with 50 mug of selenium and later given diquat (19.5 mumol/kg). Within 10 h, the selenium injection provided significant protection against diquat-induced lipid peroxidation and mortality even though this treatment resulted in no rise in glutathione peroxidase activity of liver, kidney, lung, or plasma at 10 h. This suggests that a selenium-dependent factor in addition to glutathione peroxidase exists that protects against lipid peroxidation.

Animals↗
PubMed1978

Hepatic cytosolic non selenium-dependent glutathione peroxidase activity: its nature and the effect of selenium deficiency.

Recent work had indicated the presence of a non selenium-dependent glutathione peroxidase activity in rat liver in addition to the selenium-dependent activity. The present study was undertaken to learn whether the glutathione S-transferases are reponsible for the non selenium-dependent glutathione peroxidase activity and to study the effect of selenium deficiency on those enzymes. Glutathione S-transferase B was purified by an established method using carboxymethyl cellulose ion exchange chromatography and studied. It exhibited glutathione peroxidase activity toward cumene hydroperoxide and t-butyl hydroperoxide. A limiting Km of 0.55 mM was determined for cumene hydroperoxide. Sulfobromophthalein was found to be a competitive inhibitor with respect to cumene hydroperoxide of the glutathione peroxidase activity of glutathione S-transferase B. Selenium deficiency caused an increase in glutathione S-transferase activity. These results establish that glutathione S-transferase B contributes to the non selenium-dependent glutathione peroxidase activity in rat liver and show that it increases in selenium deficiency when the selenium-dependent glutathione peroxidase is decreased.

Animals↗