Gallium poisoning: a rare case report.

The authors present a case of a college student who suffered acute gallium poisoning as a result of accidental exposure to gallium halide complexes. This is extremely rare and has never been reported in the literature. Acute symptoms after the incident, which initially presented as dermatitis and appeared relatively not life-threatening, rapidly progressed to dangerous episodes of tachycardia, tremors, dyspnea, vertigo, and unexpected black-outs. Had there been effective emergency medical care protocols, diagnostic testing, treatment and antidotes, the latent manifestations of irreversible cardiomyopathy may have been prevented. Given how quickly exposure led to morbidity, this article aims to raise an awareness of the toxic potential of gallium. This has particular relevance for workers involved in the production of semiconductors where there is a potential for accidental exposure to gallium by-products during device processing. It may also have implications for dentists who use gallium alloys to replace mercury containing amalgam. In the absence of threshold limit values and exposure limits for humans, as well as emergency medical guidelines for treatment of poisoning, the case calls on the National Institute for Occupational Safety and Health and the Occupational Safety and Health Administration to establish guidelines and medical management protocols specific for gallium.

Therapeutic potential of monoisoamyl and monomethyl esters of meso 2,3-dimercaptosuccinic acid in gallium arsenide intoxicated rats.

The dose dependent effects of monoisoamyl and monomethyl esters of meso 2,3-dimercaptosuccinic acid (DMSA) (0.1, 0.3 and 0.5 mmol kg(-1), intraperitoneally (i.p.) once daily for 5 days) to offset the characteristic biochemical, immunological, oxidative stress consequences and DNA damage (based on DNA fragmentation and comet assay) following sub-chronic administration of gallium arsenide and the mobilization of gallium and arsenic were examined. The effects of these chelators alone in normal animals too were examined on above-mentioned variables. Male Wistar rats were exposed to 10 mg kg(-1), GaAs, orally once daily for 12 weeks and were administered DMSA or two of its monoesters (monoisoamyl or monomethyl) for 5 consecutive days. DMSA was used as a positive control. DMSA and its derivatives, when given alone, generally have no adverse effects on various parameters. After 5 days of chelation therapy in GaAs pre-exposed rats, MiADMSA was most effective in the reduction of inhibited blood delta-aminolevulinic acid dehydratase (ALAD) activity and zinc protoporphyrin level while, all three chelators effectively reduced urinary ALA excretion, compared to GaAs alone exposed rats. MiADMSA was also effective, particularly at a dose of 0.3 mmol kg(-1), in enhancing the inhibited hepatic transaminase activities. Parameters indicative of oxidative stress responded less favorably to the chelation therapy, however, three chelators significantly restored the altered immunological variables. MiADMSA was relatively more effective than the other two chelators. GaAs produced significant DNA damage in the liver and kidneys and the chelation treatment had moderate but significant influence in reducing DNA damage. All three chelators significantly reduced arsenic concentration and, however, MiADMSA was more effective than the other two chelators in depleting arsenic concentration from blood and other soft tissues. A dose of 0.3 mmol kg(-1) was found to be relatively better than the other two doses examined. Gallium contents of blood and soft tissues remained uninfluenced by the chelation therapy. Significant loss of copper after MiADMSA administration, however, is of concern and requires further exploration. Additionally, further studies are required for the choice of appropriate dose, duration of treatment and possible toxic/side effects. Keeping in view the promising role of MiADMSA in the treatment of GaAs poisoning, these data will be needed for the registration of this chelating agent as licensed drug for the treatment of gallium arsenide intoxication.

Relative efficacy of chelating agents as antidotes for acute gallium nitrate intoxication.

Twelve chelating agents were administered to mice by IP injection to compare their relative effectiveness in preventing death after a single IP injection of gallium nitrate. Na2Ca-ethylenediaminetetraacetate (EDTA), Na3Ca-diethylenetriaminepentaacetate (DTPA), dimercaptosuccinic acid (DMSA), 4,5-dihydroxy-1,3-benzene-disulfonic acid (Tiron), sodium diethyldithiocarbamate (DDC), L-cysteine and sodium salicylate were not effective for acute gallium nitrate intoxication. The therapeutic indices of the effective chelators were: 25.4 (deferoxamine mesylate), 35.7 (citric acid), 42.3 (succinic acid), 52.2 (malic acid) and 111.1 (oxalic acid).