Koskinen-Kainulainen M, Luoma H, Tuomisto J
Department of Preventive Dentistry and Cariology, University of Kuopio, Finland.
Magnes Trace Elem. 1990;9(1):15-27.
The LD50 for fluoride was elevated from less than 60 mg F/kg body weight to 172 mg F/kg when magnesium (as MgCl2), equivalent to 3 times that of F, was administered by gavage 30 min after the F dose. A dose of 30 mg F/kg elevated the mean steady state of F in serum nearly 1.5-fold and in femoral bone nearly 2-fold when administered with or without the subsequent Mg dose and observed 24 h after the electrolyte dosages. Also, in 24-hour urine the mean F excretion was highest in the F and FMg groups. The total F excretion (fecal + urinary) was elevated 8- and 10-fold when fluoride was administered with or without magnesium, as compared to control levels. Magnesium administration with fluoride did not significantly modify the above mean values of the group given fluoride alone. This suggests that interference with the absorption of fluoride was not the primary protective function of magnesium against the acute toxicity of fluoride. Additional experiments, conducted to further clarify the toxic mechanism of fluoride and the protective mechanism of magnesium, resulted in the following findings: An intraperitoneal dose of 20 mg F/kg elevated fluoride concentration in serum in 1 h about 20 times compared to the controls. Magnesium injected simultaneously with fluoride did not modify the effect of fluoride alone. No significant changes were found in the concentrations of K, Mg, Na or Ca of the lung, skeletal muscle, kidney or liver after these injections except for some trend of elevation of Ca in the heart. However, after a dose of 30 mg F/kg i.p., the heart Ca/Mg mole ratio was elevated within 1 h from 0.037 to 0.194, while all of these rats died within 1 h after the injections. When magnesium, equivalent to 3 times the amount of fluoride was injected, this mole ratio was only 0.095, and all rats in this group survived over 1 h. These results suggest that the lethality of fluoride may be dominantly mediated by the elevated Ca (Ca/Mg ratio) in the heart muscle and that this is correctable by Mg.
当在给予氟剂量30分钟后通过灌胃给予相当于氟3倍量的镁（以MgCl₂形式）时，氟的半数致死量（LD50）从低于60毫克氟/千克体重提高到172毫克氟/千克体重。当给予30毫克氟/千克剂量时，无论随后是否给予镁剂量，并在给予电解质剂量24小时后观察发现，血清中氟的平均稳态水平提高了近1.5倍，股骨中氟的平均稳态水平提高了近2倍。此外，在24小时尿液中，氟组和氟镁组的氟平均排泄量最高。与对照水平相比，无论是否与镁一起给予氟，氟的总排泄量（粪便 + 尿液）都提高了8倍和10倍。与单独给予氟的组相比，同时给予氟和镁并没有显著改变上述平均值。这表明，干扰氟的吸收并非镁对氟急性毒性的主要保护作用机制。为进一步阐明氟的毒性机制和镁的保护机制而进行的额外实验得出了以下结果：腹腔注射20毫克氟/千克剂量后1小时，血清中氟浓度比对照组升高了约20倍。与氟同时注射的镁并没有改变氟单独产生的作用。除了心脏中钙有一些升高趋势外，这些注射后，肺、骨骼肌、肾脏或肝脏中的钾、镁、钠或钙浓度没有发现显著变化。然而，腹腔注射30毫克氟/千克剂量后1小时内，心脏钙/镁摩尔比从0.037升高到0.194，而所有这些大鼠在注射后1小时内死亡。当注射相当于氟3倍量的镁时，该摩尔比仅为0.095，该组所有大鼠存活超过1小时。这些结果表明，氟的致死性可能主要由心肌中升高的钙（钙/镁比值）介导，而这可通过镁来纠正。
