Comparative in vitro toxicity of cadmium and lead on redox cycling in type II pneumocytes

Abstract

Both cadmium and lead have pulmonary toxicity: cadmium can cause lung cancer, fibrosis and emphysema; lead can induce a moderate interstitial pulmonary fibrosis. Both metals give rise to depletion of glutathione and depletion of the protein-bound sulfhydryl groups, and lead to the production of reactive oxygen species. In the primary culture of type II pneumocytes, which is one of the most important cell groups from the aspect of glutathione metabolism and thus redox balance, the effect of cadmium chloride and lead nitrate upon the enzymes of the glutathione cycle, upon superoxide dismutase and upon the structure of type II pneumocytes was examined. Depending on the concentration, cadmium inhibited each of these parameters, whereas lead nitrate significantly increased the activity of glutathione reductase while inhibiting other parameters. Both metals induced damage of the membranes of type II cells, depending on the concentration, although cadmium caused significantly more damage than lead. The data obtained suggest that both substances cause an imbalance in the redox cycle and diversely affect the function and membrane structure of type II pneumocytes.

Oxidative DNA damage levels and catalase activity in the clam Ruditapes decussatus as pollution biomarkers of Tunisian marine environment

“…With respect to the gulf of Gabés (sites 4, 5 and 6), there are recent literature reports indicating high metal concentrations is soft tissues of R. decussatus (Smaoui-Damak et al, 2003;Hamza-Chaffai et al, 2003). It has been known that metals are involved in ROS generation through Fenton reactions, the inactivation of antioxidant defenses, or by inhibiting electron transport chain, allowing the transference of electrons directly to oxygen (Ochi et al, 1987;Tatrai et al, 2001). Thus, the exposure of organisms to metals can cause oxidative stress by increasing the rate of ROS production, and the increases in CAT activity seen in R. decussatus from gulf of Gabés and possibly other sites compared to control values would be a response to an increase in ROS generation due to metal exposure.…”

Endogenous lipid pneumonia in rats after subacute exposure to CdCl2

“…Damage of type I pneumocyte, hyperplasia of type II pneumocytes, and pulmonary interstitial fibrosis has been described secondary to cadmium exposure (Yamamoto, et al, 1983;Oberdöster, 1989;Tátrai, et al, 2001;Kwon, et al, 2003), and in vitro, morphological changes in the membrane of type II pneumocytes due to cadmium-inhibited protein synthesis has also been noted (Tátrai, et al, 2001). In our study, after the cadmium administration, the lungs showed an interstitial pneumonia and hyperplasia of type II pneumocytes, which is related to apoptosis of type I pneumocytes originated by oxidative stress (Kwon, et al, 2003).…”

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“…Significant changes in the band areas at 3307, 1543, 1163, 696 of liver tissue and 3364, 2926, 1741, 1653, 1543, 1456, 1394, 1163 of muscles tissue further suggested that Cd had more drastic effect on the tissue architecture as compared to Pb. In a previous study, Tatrai et al (2001) observed toxicity is the production of reactive oxygen species which further aggravate the normal homeostasis of the cells thereby affecting the biochemical integrity (Dewanjee et al 2013, Souid et al 2013. However, cells have marked defense mechanism to overcome the production of oxidatively modified protein with an increased proteolysis (Chondrogianni et al 2014).…”

“…However, each toxic metal has unique toxicity mechanism, for example Pb 2+ has the ability to compete for diverse polyvalent cations (Ca, Zn, Mg) in their binding sites (Garza et al 2006). This evolutionary characteristic of Pb 2+ may affect several physiological functions with the onset of structural and compositional change in the cells and tissues, whereas Cd has the ability to reduce the activity of glutathione reductase, which is a pre requisite for membrane integrity (Tatrai et al 2001). Thus, it is imperative to further investigate the toxicity mechanism of these metals and their interactions in details.…”