Assay for lipid peroxides in animal tissues by thiobarbituric acid reaction

The terms 'antioxidant', 'oxidative stress' and 'oxidative damage' are widely used but rarely defined. This brief review attempts to define them and to examine the ways in which oxidative stress and oxidative damage can affect cell behaviour both in vivo and in cell culture, using cancer as an example.

Biochemistry of oxidative stress

长期以来,对于肿瘤的发病机制,就存在两种意见,一种意见认为,肿瘤的发生是由于基因突变导致的遗传特性改变引起的,另一种意见认为,肿瘤的发生是由于基因表达的失调,即通过表遗传学机制引起的.只是近几十年来,由于癌基因与抑癌基因的发现及对之研究的巨大进步,使得肿瘤表遗传学的研究一直处于遗传学研究的阴影之下而已[1]。

Cancer epigenetics

Of easily readable size and presenting its material in an attractive format, this work is oriented toward the medical student. It covers the subject under major headings of splanchnic circulation, motor mechanisms, secretion, digestion, and absorption. The bibliography is brief, and controversial points generally are passed over. Although opinions differ over what the medical student should be taught and how material should be presented, coverage certainly offers an adequate background in most areas of gastrointestinal physiology. Hepatic physiology, however, is incompletely examined, and the authors seem not to have decided how to approach this complicated subject. Perhaps hepatic physiology, now so extensive, can be covered adequately only in a separate volume. Some of the material is presented and discussed in a confusing or inadequate manner, especially for a book designed as an introductory text for students. For example, the authors mention results obtained by using a Pavlov pouch, but they

Physiology of the Gastrointestinal Tract

Humans are exposed to cobalt (Co) and chromium (Cr) from industry and surgical devices, most notably orthopedic joint replacements. This review compares the potential health effects of exposure to Co and Cr contaminants from these two different sources, both in the locally exposed tissues and at sites distant to the primary exposure. Surgical implantation results largely in exposures to ions, corrosion products, and particles of Co and Cr. Industrial exposures are predominantly to metal compounds and particles. Although there are large literatures on industrial and surgical exposures to these metals, there has yet to be a systematic comparison of the two to test whether more general lessons might be learned about the human toxicology of Co and Cr. Both industrial and surgical exposures cause inflammatory and other immune reactions in the directly exposed tissues. In the lung there is a well-established risk of cancer following long-term exposures to hexavalent Cr; however, the development of sarcoma in the connective tissues adjacent to implants in response to metal particles is rare. Both types of exposure are associated with changes in the peripheral blood, including evidence of oxidative stress, and altered numbers of circulating immune cells. There is dissemination of Co and Cr to sites distant to the orthopedic implant, but less is known about systemic dissemination of these metals away from the lung. The effects of industrial exposures in the reproductive, renal, and cardiac systems have been investigated, but this has yet to be explored after surgical exposures. The form of the metal (and associated elements) in both instances is key to the toxicological effects arising in the body and further characterization of debris released from devices is certainly recommended, as is the impact of nanotoxicology on the health and safety of workers and patients. Biomonitoring schemes currently used in industry could be translated, if required, into suitable programs for orthopedic out-patients. Cross-communication between experts in industrial and occupational medicine and regulatory agencies may be useful.

A Systematic Comparison of the Actual, Potential, and Theoretical Health Effects of Cobalt and Chromium Exposures from Industry and Surgical Implants

Sodium nitrite-induced oxidative stress causes membrane damage, protein oxidation, lipid peroxidation and alters major metabolic pathways in human erythrocytes.

Effect of fasting on enzymes of carbohydrate metabolism and brush border membrane in rat intestine

Potassium bromate (KBrO3) is widely used as a food additive and is a major water disinfection by-product. It induces multiple organ toxicity in humans and experimental animals and is a probable human carcinogen. The present study reports the protective effect of dietary antioxidant taurine on KBrO3-induced damage to the rat intestine. Animals were randomly divided into four groups: control, KBrO3 alone, taurine alone and taurine+ KBrO3. Administration of KBrO3 alone led to decrease in the activities of intestinal brush border membrane enzymes while those of antioxidant defence and carbohydrate metabolism were also severely altered. There was increase in DNA damage and DNA-protein cross-linking. Treatment with taurine, prior to administration of KBrO3, resulted in significant attenuation in all these parameters but the administration of taurine alone had no effect. Histological studies supported these biochemical results showing extensive intestinal damage in KBrO3-treated animals and greatly reduced tissue injury in the taurine+ KBrO3 group. These results show that taurine ameliorates bromate induced tissue toxicity and oxidative damage by improving the antioxidant defence, tissue integrity and energy metabolism. Taurine can, therefore, be potentially used as a therapeutic/protective agent against toxicity of KBrO3 and related compounds.

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Chemoprotective effect of taurine on potassium bromate-induced DNA damage, DNA-protein cross-linking and oxidative stress in rat intestine

Mercury is among the most toxic heavy metals and a widespread environmental pollutant. Mercury chloride (HgCl2) is an inorganic compound of mercury which is easily absorbed in the gastrointestinal tract and then enters the blood where it can interact with erythrocytes. In this study, the effect of HgCl2 on human erythrocytes was studied under in vitro conditions. Erythrocytes were treated with different concentrations of HgCl2 (1–100 μM) for 1 h at 37 °C. Cell lysates were prepared and assayed for several biochemical parameters. HgCl2 treatment resulted in oxidation of ferrous iron of hemoglobin to ferric form giving methemoglobin which is inactive as an oxygen transporter. However, the activity of methemoglobin reductase was increased. Hemoglobin oxidation was accompanied by heme degradation and the release of free iron. Protein oxidation was greatly increased with a simultaneous decrease in free amino and sulfhydryl groups and glutathione content. The antioxidant power of HgCl2-treated erythrocytes was impaired resulting in lowered metal reducing and free radical quenching ability of these cells. This suggests that HgCl2 induces oxidative stress in human erythrocytes. This was confirmed when superoxide anion, hydrogen peroxide, peroxynitrite, and nitric oxide generation were found to be dose-dependently increased in HgCl2-treated erythrocytes. Glycolysis and pentose phosphate pathway, the two major pathways of glucose metabolism in erythrocytes, were also inhibited. HgCl2 treatment also inhibited the plasma membrane redox system while the activities of AMP deaminase and glyoxalase-I were increased. These results show that HgCl2 induces oxidative and nitrosative stress, oxidizes hemoglobin, impairs the antioxidant defense mechanism, and alters metabolic pathways in human erythrocytes.

Mercury chloride toxicity in human erythrocytes: enhanced generation of ROS and RNS, hemoglobin oxidation, impaired antioxidant power, and inhibition of plasma membrane redox system

Vitamin C attenuates potassium dichromate-induced nephrotoxicity and alterations in renal brush border membrane enzymes and phosphate transport in rats.

Riaz Mahmood

Papers

Sodium nitrite-induced oxidative stress causes membrane damage, protein oxidation, lipid peroxidation and alters major metabolic pathways in human erythrocytes.

Effect of fasting on enzymes of carbohydrate metabolism and brush border membrane in rat intestine

Chemoprotective effect of taurine on potassium bromate-induced DNA damage, DNA-protein cross-linking and oxidative stress in rat intestine

Mercury chloride toxicity in human erythrocytes: enhanced generation of ROS and RNS, hemoglobin oxidation, impaired antioxidant power, and inhibition of plasma membrane redox system

Vitamin C attenuates potassium dichromate-induced nephrotoxicity and alterations in renal brush border membrane enzymes and phosphate transport in rats.