Augusta A. Mylroie

Bio: Augusta A. Mylroie is an academic researcher from Chicago State University. The author has contributed to research in topics: Superoxide dismutase & Lead acetate. The author has an hindex of 3, co-authored 7 publications receiving 303 citations. Previous affiliations of Augusta A. Mylroie include Community College of Philadelphia.

Metabolic interactions between lead and copper in rats ingesting lead acetate

Abstract: The effects of Pb ingestion with and without concurrent dietary Cu supplementation were determined on parameters associated with Cu deficiency in rats fed a nutritionally adequate diet. Groups of weanling male Sprague-Dawley rats were fed a purified (AIN-′76) diet and given Pb (0 or 500 ppm) and Cu (0, 6, or 12 ppm) as the acetate salt in deionized drinking water for 5 wk. A Pb-induced Cu deficiency resulted that was characterized by decreased levels of Cu in tissue and blood, decreased activities of the Cu-dependent enzymes, ceruloplasmin (serum) and Superoxide dismutase (erythocytes), and increased concentration of Fe in liver. These effects of Pb were prevented completely or in part by concurrent Cu supplementation. The Pb-induced decrease in hemoglobin and hematocrit values and the decrease in weight gain were not prevented by Cu supplementation of the diet and can therefore be assumed to be the direct result of a toxic effect of Pb. Although Pb ingestion resulted in decreased concentration of Cu in blood and tissue, additional dietary Cu had no effect on Pb levels.

Lead-exposure of neonatal rats through maternal milk : A confounded model.

Abstract: Lead-exposed neonatal rats are frequently used as a model for plumbism in children. In most studies,PPb is administered to the dam, and it is assumed that the pups are exposed to Pb primarily from the dam's milk. Rat pups, however, are coprophagic and begin to consume the maternal feces in their second postnatal week. This experiment was designed to determine whether the maternal feces are a significant source of Pb in pups exposed via the lactating dam. Dams were administered Pb as lead acetate (PbAc), either through their drinking water (500 ppm PbAc) or through twice daily intubations (3 mg PbAc/Kg body wt) from postpartum d 1 (P1) to P21 (P0=day of birth). Control dams were administered deionized water. The dams were housed with their litters in stainless-steel hanging cages with wire-screened bottoms. Litters of exposed and control dams treated through their drinking water had access to either Pb-containing or Pb-free maternal fecal matter for 2 h/d during the late lactation period. Half of the litters from intubated dams had continuous access to maternal feces throughout the lactation period, whereas access was curtailed at P14 in the other litters. Lead content of the feces from Pb-exposed dams ranged from 1000 to 5000 μg Pb/g wet wt. At P21, Pb concentrations were 2–4 times higher in blood, brain, bone, and liver of pups that had access to Pb-contaminated feces than in pups that were exposed to Pb primarily through the mother's milk. When estimating exposure levels in pups receiving Pb through the lactating dam, coprophagy and the high content of Pb in the dam's feces must be taken into consideration.

Further studies on the effects of dietary copper deficiency on rat pancreas

Abstract: The present study was designed to obtain further information on the effect of Cu deficiency on the pancreas and on pancreatic SOD activity. In a series of experiments, groups of male weanling Sprague Dawley rats were fed either a Cu sufficient Cu or Cu deficient purified AIN-'76 diet. Cu levels were determined in blood and selected organs by atomic absorption spectrophotometry. Serum ceruloplasmin, hemoglobin and hematocrit values were determined. Aliquots of homogenized pancreas were assayed for CuSOD, MnSOD and other pancreatic enzyme activities. Although the experimental conditions appeared to be identical to those used in previous experiments, the results were different. In the experiments reported here, even though pancreatic weights decreased by week 7 relative to controls, there was no evidence of pancreatic atrophy. There was no significant decrease in CuSOD, but an unexpected increase in MnSOD activity by week 9 in rats fed Cu-deficient diet. An examination of all data indicates that the difference in results between previous experiments and those reported here was due to the varying degree of Cu deficiency produced: Cu deficiency was less pronounced in the present study.

Can antioxidant be beneficial in the treatment of lead poisoning

Abstract: Recent studies have shown that lead causes oxidative stress by inducing the generation of reactive oxygen species, reducing the antioxidant defense system of cells via depleting glutathione, inhibiting sulfhydryl-dependent enzymes, interfering with some essential metals needed for antioxidant enzyme activities, and/or increasing susceptibility of cells to oxidative attack by altering the membrane integrity and fatty acid composition. Consequently, it is plausible that impaired oxidant/antioxidant balance can be partially responsible for the toxic effects of lead. Where enhanced oxidative stress contributes to lead-induced toxicity, restoration of a cell's antioxidant capacity appears to provide a partial remedy. Several studies are underway to determine the effect of antioxidant supplementation following lead exposure. Data suggest that antioxidants may play an important role in abating some hazards of lead. To explain the importance of using antioxidants in treating lead poisoning the following topics are addressed: (i) Oxidative damage caused by lead poisoning; (ii) conventional treatment of lead poisoning and its side effects; and (iii) possible protective effects of antioxidants in lead toxicity.

Invited critical review Low level lead exposure and oxidative stress: Current opinions

Abstract: Lead continues to pose a serious threat to the health of many children as well as adults. Concern about lead exposure as a significant public health problem has increased as evidence has mounted regarding adverse health effects at successively lower levels. This issue is complicated by the fact that there is no demonstrated biological function of lead in human. Lead potentially induces oxidative stress and evidence is accumulating to support the role of oxidative stress in the pathophysiology of lead toxicity. Lead is capable of inducing oxidative damage to brain, heart, kidneys, and reproductive organs. The mechanisms for lead-induced oxidative stress include the effects of lead on membranes, DNA, and antioxidant defense systems of cells. Recent epidemiological and toxicological studies have reported that lead exposure causes several diseases including hypertension, kidney disease, neurodegenerative disease and cognitive impairment. Although all these diseases include components of oxidative stress, the relevance of oxidative stress to lead-related diseases with low lead exposure has been criticized because most of the mechanistic studies have been conducted at moderate to higher dose levels. The association between low level lead exposure and oxidative stress has not been explored systematically. The present review focuses on mechanisms for lead-induced oxidative stress and relevance of oxidative stress to lead-related human disease with low lead exposure. © 2007 Elsevier B.V. All rights reserved.

Lipoperoxidative Damage on Lead Exposure in Rat Brain and its Implications on Membrane Bound Enzymes

Abstract: We have investigated the effect of lead exposure on lipid peroxidation, a deteriorative process of the membranes, in the different regions of the brain. Lead treatment (50 mg/kg b.wt. intragastrically) for a period of eight weeks to rats resulted in a significant accumulation of lead in all the regions of brain, at maximum in hippocampus. The lipid peroxidation was accentuated following lead exposure and there was a linear correlation between the increase in lipid peroxidation and increase in lead levels (r = 0.75). The antioxidant capacity of the neuronal cells in terms of the activity of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase was diminished. Lead treatment also altered the glutathione status i.e. levels of reduced glutathione were lowered, accompanied with the accumulation of oxidized glutathione. Furthermore, the activity of glutathione reductase was significantly lowered in lead-treated animals. The activity of membrane bound enzyme acetylcholinesterase was significantly inhibited following lead exposure and there was a linear correlation between the increase in lipid peroxidation and decrease in acetylcholinesterase activity (r = -0.83). It appears from the results that lead may exert its neurotoxic effects via peroxidative damage to the membranes.