Stressor: 716
Title
Cisplatin
Stressor Overview
AOPs Including This Stressor
Events Including This Stressor
Chemical Table
User term | DTXID | Preferred name | Casrn | jchem_inchi_key | indigo_inchi_key |
---|---|---|---|---|---|
Cisplatin | DTXSID4024983 | Cisplatin | 15663-27-1 | DQLATGHUWYMOKM-UHFFFAOYSA-L | DQLATGHUWYMOKM-UHFFFAOYSA-L |
AOP Evidence
Event Evidence
Inhibition, Mitochondrial Electron Transport Chain Complexes
In Santos et al.’s (2007) study on the nephrotoxicity induced by platinum-based cisplatin, ATP synthesis was assessed by measuringkidney ATP content, and was found to be significantly decreased in the cisplatin-treated group (75% of control). They also demonstrated a decrease in mitochondrial lipid levels due to their oxidation by cisplatin, which further inhibited the mitochondrial electron transport chain. Cardiolipin levels in particular were decreased to 73% of the control group (Santos et al., 2007).
Occurrence, Kidney toxicity
Santos et al. (2007) investigated the effects of cisplatin on renal functioning in rats. They found that plasma urea and creatinine levels were significantly elevated in the rats treated with cisplatin, when compared to the control group (Santos et al., 2007).
Increase, Cytotoxicity (renal tubular cell)
Santos et al. (2007) investigated the effects of cisplatin treatment on rat kidneys and found that the treated rats had significantly elevated levels of caspase-3 activity, implying an increase in apoptosis in the treated cells.
Sprekelmeyer et al. (2017) also found that rat kidney cells treated with cisplatin showed dose dependant decreases in viability when treated with 0 to 100 μM. The IC50 value determined from this article was 17.0 μM (Spreckelmeyer et al., 2017).