Oral zinc aspartate treats experimental autoimmune encephalomyelitis (2014)
https://link.springer.com/article/10.10 ... 014-9786-8
The essential trace element zinc plays a critical role in the regulation of immune homeostasis. Zinc deficiency or excess can cause severe impairment of the immune response, which points to the importance of the physiological and dietary control of zinc levels for a functioning immune system. We previously reported that injection of zinc aspartate suppresses experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis (MS), as well as effector T cell functions in vitro. Among the preferred characteristics of novel therapeutics for the treatment of autoimmune diseases such as MS are oral availability and a tolerable effective dose to minimize side effects. In this study, we investigated whether oral administration of zinc aspartate, an approved drug to treat zinc deficiency in humans, is effective in controlling EAE at clinically approved doses. We show that oral administration of 6 µg/day [0.3 mg/kg body weight (BW)] or 12 µg/day [0.6 mg/kg BW] of zinc aspartate reduces clinical and histopathological signs during the relapsing remitting phase of the disease in SJL mice. The clinical effect in mice was accompanied by suppression of IFN-γ, TNF-α, GM-CSF and IL-5 production in stimulated human T cells and mouse splenocytes in a dose-dependent manner. Furthermore, a large array of proinflammatory cytokines was modulated by zinc aspartate exposure in vitro. These data suggest that administration of oral zinc aspartate may have beneficial effects on autoimmune diseases like MS.
Here, we measured the zinc concentrations in the plasma of naive mice and of mice in the course of EAE and found a significant reduction of zinc plasma concentrations in mice with EAE on day 21 in comparison to zinc plasma concentrations of naive mice"
Olfactory function in zinc-deficient adult mice (1989)
"Adult zinc deficiency reportedly leads to degeneration of the olfactory epithelium in the rat. Human zinc deficiency can cause reduced olfactory sensitivity. Given the importance of zinc in embryonic neural development its primary action on the adult olfactory system may be to disrupt olfactory receptor neurogenesis. We report here on the effects of zinc deficiency on the olfactory system of the adult mouse. After 42 days of dietary restriction of zinc, mice were tested behaviourally for olfactory function and general activity. Their olfactory epithelia were examined histologically using [3H]-thymidine autoradiography to identify recently-divided cells, and immunohistochemistry for olfactory marker protein to identify mature receptor neurones. Zinc deficient mice failed to show a food odour preference but they Were as active as controls and their olfactory epithelia appeared normal. Basal cell proliferation and postmitotic survival were similar to controls and the epithelia were of normal thickness and were positive for olfactory marker protein. It was concluded that zinc deficiency did not affect the turnover of cells in the olfactory epithelium. It may disrupt olfactory function through interference with zinc-containing neurones in higher olfactory centres.
The evidence for zinc involvement in human olfaction is more equivocal. Acute serum zinc loss, induced by a few days of histidine treatment, was associated with raised odour detection and recognition thresholds in six patients. Administration of zinc quickly reversed these effects (Henkin et al. 1975). In contrast, a group of 106 patients with low serum zinc and smell
dysfunction secondary to a variety of etiological factors, were not helped by zinc sulphate treatment (Henkin et al. 1976).
The results indicate that zinc deficiency disrupted the sense of smell of adult mice."