Lithium from breast-milk inhibits thyroid iodine uptake and hormone production, which are remedied by maternal iodine supplementation.

BACKGROUND: Lithium is especially taken as a maintenance medication for Bipolar Disorder. In women with bipolar disorder, lithium is often effective during postpartum period, but breast-feeding for medicated mothers is controversial because of harmful effects for her child. At present, the biological mechanisms of lithium are not well-understood, affecting its usage and overall health implications. PROCEDURE: We developed a rat lithium and breast-feeding model at human therapeutic levels to study the effects of lithium exposure through breast-milk on pups' thyroid function. Novel laser analytical spectroscopy, along with traditional blood and immunohistochemical tests, were applied to further investigate the mechanisms behind the thyroid dysfunction. Maternal iodine supplementation was evaluated as a therapeutic method to address the pups' thyroid dysfunction. RESULTS: Pups exposed to lithium via breastmilk, even with the dam on a sub-therapeutic level, experienced weight gain, reduced blood thyroxine (T4 ), and elevated blood urea nitrogen, indicating effects on thyroid and kidney function. We show that lithium inhibited iodine uptake by thyroid follicles, initiating a mechanism that reduced iodination of tyrosine, thyroglobulin cleavage, and thyroid hormone production. Importantly, infant thyroid function can be significantly improved by administering supplementary iodine to the medicated dam's diet during breast-feeding. CONCLUSION: These results elucidate the mechanisms of lithium in thyroid function, provide valuable information on use postpartum, and suggest a clinically applicable remedy to side-effects. The results are particularly important for patients (and their infants) who respond well to lithium and need, or choose, to breast-feed.

Single red blood cell analysis reveals elevated hemoglobin in poikilocytes.

Abnormally shaped red blood cells (RBCs), called poikilocytes, can cause anemia. At present, the biochemical abnormalities in poikilocytes are not well understood. Normal RBCs and poikilocytes were analyzed using whole-blood and single-cell methods. Poikilocytes were induced in rat blood by intragastrically administering titanium dioxide (TiO2) nanoparticles. Complete blood count and inductively coupled plasma mass spectrometry analyses were performed on whole-blood to measure average RBC morphology, blood hemoglobin (HGB), iron content, and other blood parameters. Follow-up confocal Raman spectroscopy was performed on single RBCs to analyze cell-type-specific HGB content. Two types of poikilocytes, acanthocytes and echinocytes, were observed in TiO2 blood samples, along with normal RBCs. Acanthocytes (diameter 7.7 ± 0.5 µm) and echinocytes (7.6 ± 0.6 µm) were microscopically larger (p < 0.05) than normal RBCs (6.6 ± 0.4 µm) found in control blood samples (no TiO2 administration). Similarly, mean corpuscular volume was higher (p < 0.05) in TiO2 whole-blood (70.70 ± 1.97 fl) than in control whole-blood (67.42 ± 2.03 fl). Poikilocytes also had higher HGB content. Mean corpuscular hemoglobin was higher (p < 0.05) in TiO2 whole-blood (21.84 ± 0.75 pg) than in control whole-blood (20.8 ± 0.32 pg). Iron content was higher (p < 0.001) in TiO2 whole-blood (697.0 ± 24.5 mg / l) than in control whole-blood (503.4 ± 38.5 mg / l), which supports elevated HGB as iron is found in HGB. HGB-associated Raman bands at 1637, 1585, and 1372 cm - 1 had higher (p < 0.001) amplitudes in acanthocytes and echinocytes than in RBCs from control blood and normal RBCs from TiO2 blood. Further, the 1585-cm - 1 band had a lower (p < 0.05) amplitude in normal RBCs from TiO2 versus control RBCs. This represents biochemical abnormalities in normal appearing RBCs. Overall, poikilocytes, especially acanthocytes, have elevated HGB.