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The effect of cadmium (Cd) exposure through drinking water on lipid status in mouse peritoneal macrophages (pM) was studied. After 2 months, adult male Balb/c mice that had drunk water with 15 ppm of Cd, showed tissue damage mediated by oxidative stress, as assessed by serum measuring of tissue damage and lipoperoxidation indicators. Resident pM obtained from Cd-exposed mice showed diminution in total lipids, total cholesterol, free cholesterol/esterified cholesterol ratio (FC/EC) and phospholipids in relation to control pM. On a percentage basis, the phospholipid composition showed that phosphatidylcholine (PC) and phosphatidylglycerol decreased, phosphatidylethanolamine (PE) increased, while phosphatidylinositol, sphingomyeline and phosphatidylserine did not change. The incorporation in vitro of [14C]-methyl-choline and [14C]-phosphorylcholine, as well as the activity of regulatory enzyme CTP-phosphocholine cytidylyltransferase, decreased in PC after 60 min. The incorporation of [14C]-linoleic acid increased after 1 h and the incorporation of [14C]-ethanolamine increased after 90 min in PC. The incorporation in vitro of [3H]-cholesterol in total lipids decreased after 120 min of incubation. Besides, the stearic acid and arachidonic acid content increased, while the contents of palmitoleic acid and linoleic acid decreased. Chronic Cd exposure alters the lipid composition in resident pM of Balb/c mice.

Different protocols of cadmium (Cd) exposure in non-cytotoxic conditions (i.e. 10 microM Cd for 18 h), and their effect on nitric oxide (NO) generation induced by NO inductor agents (NOIA) in peritoneal macrophages (pM) were studied. In all cases, NOIA (i.e. bacterial lipopolysaccharide [LPS], phorbol ester [PMA], okadaic acid [OA] or their combinations [LPS/OA] and [LPS/PMA]) were added at the beginning of the first incubation, only. Simultaneously exposure with 10 microM Cd enhanced NO generation and inducible NO synthase (iNOS) expression evoked by LPS, OA, PMA; those induced by LPS/PMA were not modified; and those caused by LPS/OA in relation to culture without Cd (medium) decreased. Double incubation, either with or without Cd (Cd+Cd or medium+medium), or Cd added at the start of the first or second incubation only (Cd+medium or medium+Cd), were tested. After the second incubation, medium+Cd protocol produced the highest NO generation in relation to other exposure protocols. When NO production was measured at the end of the second incubation, Cd+medium protocol enhanced NO production induced by OA, and LPS/OA, while medium+Cd protocol enhanced the response to LPS, PMA, and LPS/OA, in both cases in relation to the first incubation. Cd+Cd incubation protocol decreases the response to all NOIA in relation to another protocols. Cd effect on NO generation in macrophages is dependent on protocol and timing of exposure.

The effects of cadmium (Cd) in non-cytotoxic conditions on the nitric oxide (NO) production in peritoneal macrophages (pM) were studied. Peritoneal macrophages from Balb/c mice were incubated over 18 h with 5, 10, 20, or 25 microM Cd2+ (as CdCl2 21:2 H2O) in the culture medium. Concentrations of 20 microM Cd2+ and over had cytotoxic effects, measured by MTT assay. Cell viability with 10 microM Cd2+ in the medium was above 90% after 18 h of incubation, and above 80% after 72 h. At this same Cd2+ concentration, NO production increased from 6 to 18 h. At 24 h production decreased but was still above control levels. At 48 h production NO was near control levels, and continued to decrease until the end of the experiment (72 h). NO levels produced with Cd2+ concentrations of 5, 10 and 20 microM in the medium were above the control at 18 h. NO production and lipoperoxidation increased simultaneously after 18 h with 10 microM of Cd in the medium. Amounts of inducible nitric oxide synthase (iNOS) protein and iNOS activity also increased. At a concentration of 10 microM Cd has a biphasic effect on NO production over time.