Relation between lipid peroxidation and inflammation in the pulmonary toxicity of cadmium

Abstract

Lipid peroxidation (LPO), measured as thiobarbituric acid reactive substances (TBARS), was evaluated in lungs of rats 24 h after intraperitoneal injection of 50, 250, and 1000 micrograms Cd/kg body weight as CdCl2. In order to gain some insight into possible causative factors responsible for these oxidative phenomena, the redox-active elements iron (Fe) and copper (Cu), and total lung protein content (an indication of pulmonary inflammatory processes) were also measured. Results obtained demonstrate a similar dose-related, non-linear evolution of total lung TBARS and total lung protein as a function of increasing lung Cd concentrations. Standardization of total lung TBARS to lung protein content further resulted in a linear relationship with lung Cd concentrations, thus suggesting a possible cause-effect relationship between these parameters. No statistically significant association was observed between the dose-related evolution of lung TBARS, and iron (Fe) and copper (Cu) after Cd exposure. The results obtained provide support for the possible involvement of inflammatory phenomena as the most likely events responsible for the generation of LPO in lung tissue following acute exposure to Cd salts.

Cadmium Toxicity Revisited: Focus on Oxidative Stress Induction and Interactions with Zinc and Magnesium

“…The author described Cd-induced production of reactive oxygen species (ROS) through interaction with critical subcellular sites such as mitochondria, peroxisomes, and microsomes, that resulted in the generation of free radicals and LPO in subcellular membranous structures. Production of ROS has been reported later in a variety of cell culture systems, as well as in intact animals via all routes of exposure (34)(35)(36)(37). We also found early signs of oxidative stress in the liver of mice exposed to a single oral Cd dose (20 mg kg -1 b. w. in the form of CdCl 2 ) through increased LPO level, expressed as malondialdehyde (MDA) after 6 h, 12 h, and 24 h (38).…”

COX-2 is associated with cadmium-induced ICAM-1 expression in cerebrovascular endothelial cells

“…It has been well documented that inflammatory brain injury is associated with disruptions in BBB which allow both an increased number of immune cells and macromolecules access to the brain extracellular fluid and the development of cerebral edema (Iadecola and Alexander, 2001;Wyss-Coray and Mucke, 2002) and prostaglandins such as PGE 2 and PGF 2␣ are linked to alterations in BBB integrity during inflammation in CNS (Mark et al, 2001). Cd causes oxidative stress and inflammations in various tissues, which are important processes operating in Cd-induced pathological conditions (Manca et al, 1994;Stohs et al, 2000). Cd induces COX-2 expression and enhances lipid peroxidation and PGE 2 synthesis in several experimental models (Romare and Lundholm, 1999;Ramirez and Gimenez, 2003).…”

Protective effects of oestradiol against cadmium-induced changes in blood parameters and oxidative damage in rats

“…•-), hydrogen peroxide (H 2 O 2 ), and hydroxyl radical (•OH) (8,9). This in turn leads to increased lipid peroxidation, DNA damage, protein oxidation, and eventually to cell dysfunction and necrosis (10).…”