When garlic (Allium sativum) was administered to rat per os simultaneously with cadmium, methylmercury and phenylmercury to detect the protective effect against the heavy metal poisoning, accumulation of heavy metals in liver, kidneys, bone and testes were decreased, and histopathological damages and the inhibition of serum alkaline phosphatase activities by heavy metals were reduced. Such effect of garlic was not shown in the 1.7% garlic treated group and most remarkable in the 6.7% garlic treated group. The protective effect of garlic was superior to those of 2,3 dimercapto-1-propanol (BAL) and D-penicillamine (PEN), and nearly similar to those of 2,3-dimercaptosuccinic acid (DMSA) and N-acetyl-DL-penicillamine (APEN), the current remedies, while garlic was not effective as a curative agent for heavy metal poisoning. The excretion of cadmium was enhanced, more through feces than urine by garlic but the effect to the urinary excretion of cadmium was not significant comparing with DMSA or APEN when cadmium was ip injected in the first 3 days during the 12 days of oral administration of DMSA, APEN or garlic.
Animals ; Cadmium/metabolism ; Cadmium Poisoning/metabolism/*prevention & control ; *Garlic ; Male ; Mercury/metabolism ; Mercury Poisoning/metabolism/*prevention & control ; *Plants, Medicinal ; Rats ; Rats, Inbred Strains ; Tissue Distribution

OBJECTIVETo investigate the protective effects of quercetin on cadmium-induced cytotoxicity in primary cultures of rat proximal tubular (rPT) cells.

METHODSPrimary cultures of rPT cells undergoing exponential growth were incubated with 1.0 μg/mL quercetin and/or cadmium (2.5, 5.0 μmol/L), in a serum-free medium at 37 °C at different time intervals. Commercial kits were used and flow cytometric analyses were performed on rPT cell cultures to assay apoptosis and oxidative stress.

RESULTSExposure of rPT cells to cadmium acetate (2.5, 5.0 µmol/L) induced a decrease in cell viability, caused an increase in apoptotic rate and apoptotic morphological changes. Simultaneously, elevation of intracellular reactive oxygen species, malondialdehyde and calcium levels, depletion of mitochondrial membrane potential and intracellular glutathione, and inhibition of Na+, K+-ATPase, Ca2+-ATPase, glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) activities were revealed during the cadmium exposure of rPT cells. However, simultaneous supplementation with 1 µg/mL quercetin protected rPT cells against cadmium-induced cytotoxicity through inhibiting apoptosis, attenuating lipid peroxidation, renewing mitochondrial function and elevating the intracellular antioxidants (non-enzymatic and enzymic) levels.

CONCLUSIONThe present study has suggested that quercetin, as a widely distributed dietary antioxidant, contributes potentially to prevent cadmium-induced cytotoxicity in rPT cells.

Animals ; Antioxidants ; pharmacology ; therapeutic use ; Apoptosis ; drug effects ; Cadmium ; toxicity ; Cadmium Poisoning ; prevention & control ; Calcium ; metabolism ; Calcium-Transporting ATPases ; metabolism ; Cells, Cultured ; Kidney Tubules, Proximal ; drug effects ; metabolism ; Malondialdehyde ; metabolism ; Membrane Potential, Mitochondrial ; drug effects ; Quercetin ; pharmacology ; therapeutic use ; Rats ; Reactive Oxygen Species ; metabolism ; Sodium-Potassium-Exchanging ATPase ; metabolism