Abstract
Excessive manganese (Mn) exposure may adversely affect the central nervous system, and cause an extrapyramidal disorder known as manganism. The glutamine (Gln)/glutamate (Glu)–γ-aminobutyric acid (GABA) cycle and thyroid hormone system may be involved in Mn-induced neurotoxicity. However, the effect of Mn on the Gln/Glu–GABA cycle in the serum has not been reported. Herein, the present study aimed to investigate the effects of sub-acute Mn exposure on the Gln/Glu–GABA cycle and thyroid hormones levels in the serum of rats, as well as their relationship. The results showed that sub-acute Mn exposure increased serum Mn levels with a correlation coefficient of 0.733. Furthermore, interruption of the Glu/Gln–GABA cycle in serum was found in Mn-exposed rats, as well as thyroid hormone disorder in the serum via increasing serum Glu levels, and decreasing serum Gln, GABA, triiodothyronine (T3) and thyroxine (T4) levels. Additionally, results of partial correlation showed that there was a close relationship between serum Mn levels and the detected indicators accompanied with a positive association between GABA and T3 levels, as well as Gln and T4 levels in the serum of Mn-exposed rats. Unexpectedly, there was no significant correlation between serum Glu and the serum T3 and T4 levels. In conclusion, the results demonstrated that both the Glu/Gln–GABA cycle and thyroid hormone system in the serum may play a potential role in Mn-induced neurotoxicity in rats. Thyroid hormone levels, T3 and T4, have a closer relationship with GABA and Gln levels, respectively, in the serum of rats.
Highlights
Manganese (Mn), an essential element, acts as a key co-factor in multiple critical enzymatic reactions, including those involved in the metabolisms of lipid, protein, carbohydrate and amino acid neurotransmitter, etc. [1]
The present study showed that Mn chloride treatment for 4 weeks interfered on the balance of thyroid hormones, as indicated by a decrease in the serum T4 and T3 levels, the serum T3 and T4 levels showed a similar pattern in the present study, as T3 and T4 were decreased in all treatment groups (Figure 2)
The results showed that all treatment groups showed a decrease in the serum Gln and GABA levels of rats, while serum Glu levels slightly increased in the 15 and 30 mg/kg Mn groups compared to the control, suggesting that the serum Gln and GABA levels were more sensitive to Mn exposure than serum Glu levels (Figure 3)
Summary
Manganese (Mn), an essential element, acts as a key co-factor in multiple critical enzymatic reactions, including those involved in the metabolisms of lipid, protein, carbohydrate and amino acid neurotransmitter, etc. [1]. Manganese (Mn), an essential element, acts as a key co-factor in multiple critical enzymatic reactions, including those involved in the metabolisms of lipid, protein, carbohydrate and amino acid neurotransmitter, etc. The diet, natural presence in the environment, and anthropogenic contaminations of Mn are the main sources of environmental Mn exposure in general populations [2]. Unlike other essential trace elements (e.g., zinc and iron), human dietary Mn deficiency has not been documented [1], and the neurotoxicity of Mn is more prevalent in human populations [3]. Excessive environmental Mn exposure may induce neurotoxicity referred to as manganism [4]. Manganism is characterized by psychiatric disturbances and an extrapyramidal disorder similar to those observed in Parkinson’s disease (PD) as first described by Couper in 1837. An epidemiologic study found that higher Mn concentrations in drinking water are closely related
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