Monoisoamyl ester of DMSA reduces Hg(NO3)2 retention in rats: 2. Chelation therapy during lactation

Abstract

Two chelating agents meso‐2,3‐dimercaptosuccinic acid (DMSA) and monoisoamyl ester of DMSA (Mi‐ADMS) were compared in their efficiency to reduce inorganic mercury retention in dams and pups during lactation. Mercury‐203 and chelating agents DMSA, or Mi‐ADMS, in two doses of 0.5 mmol/kg each, were administered intraperitoneally to lactating dams as early treatment (0.5 and 24 h after 203Hg). Whole body retentions of 203Hg in dams and pups were measured daily during the 7‐day experiment. Results showed that whole body retention of mercury in dams decreased at a higher rate in the two experimental groups than in controls. At all intervals, values of the Mi‐ADMS treated group were lower than those in the DMSA group. In pups, the whole body retention of mercury increased during the first 2 days in all groups. Third day onward, the retention levels in pups of treated dams were lower than in control. From the 4th through 7th days, pups from dams treated with Mi‐ADMS had significantly lower mercury retention than pups from dams treated with DMSA. At the end of the experiment, retention of 203Hg in the whole body and tissues (gut, liver, kidney, brain, and pelt) of DMSA or Mi‐ADMS treated dams was reduced to 26–67% and 3–23% of control values, respectively. In suckling pups, whole body 203Hg retention values (after DMSA or Mi‐ADMS treatment of their dams) were reduced to 51% and 32% of control values, respectively. These effects in pups were due to lower 203Hg retention in dams resulting from chelation treatment and not because of the transfer of chelating agents through breast milk to pups. J. Trace Elem. Exp. Med. 10:183–190, 1997. © 1997 Wiley‐Liss, Inc.

Lactating and nonlactating rats differ to renal toxicity induced by mercuric chloride: the preventive effect of zinc chloride

“…In fact, during lactation, the biological half‐time of inorganic mercury decreases by 50% because of a higher rate of excretion (i.e. 3·5 days in lactating rats compared with ~7 days in nonlactating adult female) . One important mechanism that could help us to explain at least in part the reduced toxicity of mercury in lactating rats is the increase in MT synthesis during this period .…”

“…3·5 days in lactating rats compared with 7 days in nonlactating adult female). 16,17 One important mechanism that could help us to explain at least in part the reduced toxicity of mercury in lactating rats is the increase in MT synthesis during this period. 50 In our study, lactating rats were exposed to HgCl 2 close to the period of lactation (midlactation) that is recognized as being the peak period of MT synthesis in rodents.…”

“…10,11 These changes may certainly influence the distribution and elimination of chemical compounds. [12][13][14] In fact, the Hg biological half-time decreases by 40% both in humans and animals exposed to methyl mercury 15 and by 50% in animals exposed to inorganic mercury 16,17 during lactation. One study with female Wistar rats demonstrated that lactation delayed the onset of weight loss, shortened the time between the end of treatment and the onset of weight gain, accelerated the elimination of mercury from the whole body and prevented the development of severe coordination disorders after methyl mercury intoxication.…”