Renal dysfunction associated with contrast media (CM) administration is gen
erally attributed to reduced renal blood flow. Studies, however, also sugge
st direct tubular effects of CM, whose mechanisms remain unclear. This stud
y was conducted to assess the chemotoxic effects of iopamidol, a prototypic
CM, on a porcine proximal tubule (PT) cell line, LLC-PK1 cells. Results in
dicate that iopamidol did not affect cell viability (determined by trypan b
lue exclusion and fluorescein staining), but did reduce cell proliferation.
Moreover, iopamidol altered mitochondrial function, as determined by 3-(4,
5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction and
mitochondrial membrane potential. Decreased MTT reduction was evident with
all CM tested, and its rapid recovery after CM removal suggests that inhib
ition of mitochondrial function is reversible. Injury to PT cells by iopami
dol is supported by the fact that CM increase extracellular adenosine, an i
ndicator of cellular stress. This study provides greater insight into the m
echanism underlying the nephrotoxicity induced by contrast in patients and
explains the reversibility of this toxicity.