Changes in Antioxidant Lung Protection after Single Intra-tracheal Cadmium Acetate Instillation in Rats

Abstract

<jats:p> One-hundred male white rats were given a single intratracheal dose of 0, 5 mg kg<jats:sup>-1</jats:sup> cadmium acetate. There was a fall in catalase (CAT) and superoxide dismutase (SOD) in lung homogenate throughout the 30 d after treatment. Non-protein sulphhydryl (NPSH) content, glucose-6-phosphate dehydrogenase (G-6-PD) and glutathione peroxidase (GP) were all increased from days 5 to 15. There was an increase in lactate dehydrogenase (LDH) and protein in bronchoalveolar lavage fluid (BALF) and in the relative weight of the lungs which provide evidence of severe toxic lesions of the lungs. Increased lipid peroxidation provoked by the reduced lung antioxidant protective capacity may be an important mechanism in the pulmonary damage caused by cadmium. </jats:p>

EFFECTS OF CADMIUM ON GROWTH AND SUPEROXIDE DISMUTASE ACTIVITY OF THE MARINE MICROALGA TETRASELMIS GRACILIS (PRASINOPHYCEAE)1

“…In fact, studies done mainly with mammals have shown that the toxicity of many heavy metals such as lead, cobalt, mercury, nickel, and cadmium is related to an increase of ROS. Studies with adult white rats exposed to cadmium revealed pulmonary lesions, lung edema, and cardiotoxic effects manifested by increased lipid peroxidation and histopathological alterations associated with reductions of SOD, catalase, and glutathione peroxidase activities in such tissues (Jamal and Smith 1985, Ja-ma1 and Sprowls 1987, Salovsky et al 1992, Kostic et al 1993). Cultures of Chinese hamster ovary cells showed clastogenicity and generation of several ROS in response to cadmium exposure (Ochi et al 1987).…”

“…Recently, toxicological studies have suggested that cadmium could affect the antioxidant protection system of different tissues of both animals (Dudley et al 1982, Lee and White 1983, Salovsky et al 1992 and some algae (Reed and Gadd 1990). In the presence of cadmium, there is an increase in cell pro-duction of reactive oxygen species (ROS) such as superoxide anion (02-), hydroxyl radicals (OH-), hydrogen peroxide (H202), and singlet oxygen (*02), which are known to cause peroxidation of membrane lipids, depolymerization of polysaccharides, protein denaturation, and DNA damage, among other deleterious effects that lead to cell death (Halliwell and Gutteridge 1991).…”

Differential induction of proteins in Anopheles gambiae sensu stricto (Diptera: Culicidae) larvae in response to heavy metal selection

“…The heavy metal tolerance is both metal and concentration dependent (Rayms-Keller et al, 1998). The tolerance is achievable at molecular level by transcription of various genes encoding for defence and repair proteins, including immediate early genes, p53, metallothioneins, glutathione and heatshock proteins (Maroni and Watson, 1985;Salovsky et al, 1992;Abe et al, 1994;Matsuoka and Call, 1995;Ovelgonne et al, 1995;Bagchi et al, 1996;Hechtenberg et al, 1996;Beyersmann and Hechtenberg, 1997;Shimizu et al, 1997;Liao and Freedman, 1998;Kim et al, 2000;Stohs et al, 2001).…”

Cadmium‐induced gene expression is regulated by MTF‐1, a key metal‐responsive transcription factor

“…Cadmium has been shown to affect the steady-state levels of the mRNAs encoding metallothionein (Hamer, 1986), heme oxygenase (Alam et al, 1989), y-glutamylcysteine synthetase (Hatcher et al, 1995), low and high molecular weight heat shock proteins (Wiegant et al, 1994) and ubiquitin (Muller-Taubenberger et al, 1988). In addition, increment of in superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase activities are observed following cadmium exposure in cultured cells and whole animals (Kostic et al, 1993;Salovsky et al, 1992). Using suppression subtractive hybridization (SSH) technique to screen the genes expressed upon cadmium exposure in COS-7 cells, five members of the heat shock protein (hsp) family -hsp10, 40, 60, 70 and 89oc were determined (Lee et al, 2002).…”