Joseph Kyle

Bio: Joseph Kyle 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 2, co-authored 4 publications receiving 264 citations.

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.

Pancreatic Superoxide Dismutase Activity in the Copper-Depleted Rat

Abstract: Since Cu deficiency in rats is accompanied by progressive atrophy of pancreatic tissue (2, 6–8), this study was designed to investigate the role of the Cu-dependent enzymes superoxide dismutase (CuSOD) and cytochrome oxidase and the Mn-dependent enzyme superoxide dismutase (MnSOD) in this process. Superoxide dismutase catalyzes the dismutation of the superoxide radical anion (O2 −) to O and H2O2 and is considered to have an important role in protecting cells against direct and indirect oxidative damage (4, 5). The cytotoxicity of O2 − has been ascribed to the secondary production of highly reactive intermediates, such as hydroxy radicals (4).

Superoxide Dismutase Activity of Heart and Liver Tissue from Copper Deficient Rats

Abstract: Superoxide dismutase (SOD) is considered to have an important role in protecting cells against direct and indirect oxidative damage1–3. Total SOD activity is the result of the activities of a copper dependent enzyme (CuSOD), present primarily in the cytoplasm, and a manganese dependent enzyme(MnSOD), localized in the mitochondrial matrix4 The catalytic activity of CuSOD is inhibited by cyanide and this property is used to distinguish it from MnSOD.5

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.