Mammalian cell cultures were used to determine the capacity of antidot
es to modify (a) lead uptake, (b) lead toxicity and (c) lead release f
rom cells, The following chelating agents were tested: Na, Ca-ethylene
diaminetetraacetic acid (EDTA), diethylenetriaminepentaacetic acid (DT
PA), nitriloacetic acid, ethylene glycol-bis(aminoethyl)tetraacetic ac
id (EGTA), D,L-mercaptosuccinic acid (MSA), meso-2,3-dimercaptopropane
succinic acid (DMSA), D,L-2,3-dimercaptopropane-1-sulfonic acid (DMPS)
, penicillamine (PA), N-acetylpenicillamine (NAPA), and diethylcarbodi
thioate (DDTC), The following vitamins were tested: thiamine (B-1), ri
boflavine (B-2), pyridoxine (B-6), cobalamin (B-12) and ascorbic acid
(BC), Inhibition of lead uptake was produced by EDTA, EGTA, DMSA, DMPS
, MSA, PA, NAPA and vitamins B-1, B-6 and C, vitamins B-2 and B-12 bei
ng ineffective, The same compounds reduced lead cytotoxicity, Interest
ingly DDTC and DTPA increased lead uptake, but did not exacerbate lead
toxicity, Significant release of lead from preloaded cells was caused
by DTPA, NAPA, DMPS and PA, while the other chelators were ineffectiv
e.