Abstract Cadmium (Cd) is one of the most important heavy metal environmental toxicants. It alters a wide variety of cellular and biochemical processes. The objective of this work was to study DNA damage and recovery after acute and chronic CdCl 2 treatment in a human fetal hepatic cell line (WRL-68 cells). Using the alkaline microgel electrophoresis assay that detects DNA single-strand breaks and/or alkali-labile sites in individual cells, we evaluated for levels of DNA damage. The mean migration length in control cells was 35.37±1.43 μm (8% damaged cells), whereas the mean migration in cells treated with 0.005 μM CdCl 2 for 3 h (acute low dose) was 65.87±2.07 μm (88% damaged cells). Treatment with 0.01 μM CdCl 2 for the same time (acute high dose) increased the mean migration length to 125.79±2.91 μm (92% damaged cells). However, a 0.005 μM CdCl 2 treatment for 7 days (chronic treatment) only increased 65% DNA migration to 58.38±2.59 μm (88% damaged nucleus). Lipoperoxidative damage expressed as malondialdehyde (MDA) production per milligram of protein was 15.7±2.6 for control cells, whereas in Cd-treated cells the values were 20.2±2.4 (acute low dose), 22.9±2.2 (acute high dose), and 22.6±2.1 (chronic treatment). To study the repair of DNA damage, cells were washed with 0.01 μM meso-2,3-dimercaptosuccinic acid (DMSA), and fresh Dulbecco's modified essential medium (DMEM) added. The percentage of damaged cells diminished after 90 min, with DNA migration returning to control values by 120 min. Cd treatment produced DNA single-strand breaks and the damage was greater in acute high dose treated cells. Lipid peroxidation values did not correlate with DNA single-strand breaks.