The uptake and distribution of selected heavy metals were followed and related to cytotoxicity using various parameters of proliferation and viability of cultured cells. The effects of short-term lead exposure on DNA synthesis were reversible, indicating that lead does not significantly influence genetic cellular function. In contrast, nickel effects persisted, indicating that DNA is one of the main nickel targets. Heavy metals affected all cycle phases, but those related to preparation and commencement of DNA synthesis were the most susceptible. Tolerance appeared in chronic exposure to lead and cadmium. Lead combined with X-rays had additive effect, while manganese acted synergistically and appeared to inhibit the DNA repair processes. Zinc and manganese showed a protective effect against the toxic effects of cadmium. Similar antagonistic interaction was seen for nickel v. manganese cytotoxicity. This model system makes it possible to compare heavy metal effects at the cellular level and to identify cellular targets and metabolic processes.
展开▼
