Effect of lead on proliferation, oxidative stress and genotoxic damage of 3T3-L1 fibroblasts

Lead (Pb) is an environmental and industrial contaminant that still represents a public health problem. In this paper, we investigated the effect of Pb on proliferation, lipid peroxidation and the number of micronucleated cells in exponentially growing 3T3-L1 fibroblasts, a cell line previously used to evaluate different environmental contaminants. We found that Pb (10 μM or higher) was able to inhibit proliferation of exponentially growing cells after 24-h treatment, which was evaluated by the MTT assay and cell counting in Neubauer chamber, but cell survival was not affected according to the trypan blue exclusion assay. On the other hand, Pb was able to increase lipid peroxidation and the number of micronucleated cells, which are indicative of oxidative stress and genotoxic damage respectively. We also found that removal of Pb after 24-h treatment allowed cells to recover proliferation. Our results indicate that Pb was able to induce oxidative stress and genotoxicity in this cell line under standardized conditions, which supports the involvement of Pb in similar effects observed in human exposed to this heavy metal. In addition, Pb inhibits proliferation of exponentially growing fibroblasts but cells resume proliferation after removal of this metal, which suggests that it is important to move away Pb-exposed individuals from the source of contamination.

Oxidative Stress After Three Different Intensities of Running

In 8 trained subjects (T) and 9 untrained subjects (UT), lipid peroxidation (LPO), total antioxidant capacity (TRAP), superoxide dismutase, catalase, and glutathione peroxidase (GPx) activities were measured in the blood before and after three different intensities of exercise on the treadmill, determined from ventilatory threshold and maximal oxygen uptake data, obtained from a maximal aerobic power test. In plasma, LPO decreased from 3589 ± 193 to 3274 ± 223 cps•mg Hb−1(p < 0.05), and TRAP increased from 304 ± 45 to 384 ± 57 µmol•L−1trolox (p < 0.05) after high intensity exercise in T. GPx activity increased in the T group as compared to the UT group, after exercise in moderate (25.90 ± 3.79 to 15.05 ± 3.23 nM•min−1•mg protein−1) and high (21.75 ± 4.91 to 12.1 ± 2.46 nM•min−1•mg protein−1) intensities (p < 0.05). Superoxide dismutase activity increased after exercise at low (8.35 ± 0.85 to 9.23 ± 1.03 U SOD•mg protein−1) and moderate (8.89 ± 0.98 to 10.44 ± 0.86 U SOD•mg protein−1) intensity in UT (p < 0.05). There were no changes in catalase activity. These findings indicate that exercise in this model did not increase lipid peroxidation, probably because of the alterations in TRAP and enzymatic antioxidants. Key words: free radicals, lipid peroxidation, erythrocytes, antioxidant enzymes, exercise

Skeletal muscle ischemia and reperfusion in rats increase lipid peroxidation in rats

PURPOSE: To determine the effects of 30 minutes of ischemia followed by 30 minutes of reperfusion in skeletal muscle of rats receiving three different diets (supplemented, normal and vitamin E deficient) on lipoperoxidation (LP). METHODS: LP measured by TBARS levels, and plasma and hepatic concentrations of vitamin E measured by HPLC. RESULTS: The deficient group presented higher lipoperoxidation levels in muscle compared to the control and supplemented groups. CONCLUSION: Supplementation with vitamin E decrease the free radicals production in ischemia/reperfusion in skeletal muscle of rats.