Vitamin B complex in treatment of cadmium intoxication.
The effect of vitamin B-complex on cadmium nephrotoxicity and hepatotoxicity was investigated in rats. The administration of Cd (3 mg per kg, s.c., three days) increased the urinary excretions of lactic dehydrogenase (LDH), glutamic oxalacetic transaminase (GOT), and total proteins, decreased renal activities LDH and GOT and increased concentration in kidney tissue of Cd, Cu, and Zn, Cadmium also increased serum BOT and glutamic pyruvic transaminase (GPT), decreased hepatic activities of GOT and GPT, and increased hepatic levels of Cd and Zn. The supplementation of vitamin B-complex (10 mg per kg, orally) simultaneously with Cd caused less marked biological alterations. Cadmium concentration in renal tissue was significantly less on the eighth day whereas the hepatic level of Cd was unaffected by vitamin supplementation. The protective effect of vitamin B-complex in Cd toxicity may be attributed to the interference by the constituents of vitamin B-complex in body absorption of Cd, possibly through forming readily excretable complexes. The results suggest that Cd toxicity can be reduced by vitamin B-complex supplementation.
D000410:Alanine Transaminase / Q000378:metabolism / Q000652:urine; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism / Q000652:urine; D002104:Cadmium / Q000032:analysis; D002105:Cadmium Poisoning / Q000188:drug therapy*; D003300:Copper / Q000032:analysis; D007668:Kidney / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism / Q000652:urine; D008099:Liver / Q000378:metabolism; D008297:Male; D051381:Rats; D014803:Vitamin B Complex / Q000627:therapeutic use*; D015032:Zinc / Q000032:analysis
D002104:Cadmium; D014803:Vitamin B Complex; D003300:Copper; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D015032:Zinc