Severe Zinc Deficiency Causes the Loss and Apoptosis of Olfactory Ensheathing Cells (OECs) and Olfactory Deficit
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Severe Zinc Deficiency Causes the Loss and Apoptosis of Olfactory Ensheathing Cells (OECs) and Olfactory Deficit Yu Jiang 1 & Lingqi Gu 2 & Zilin Zhang 1 & Jianya Zhao 1 & Chunhua Wan 1 Received: 10 May 2020 / Accepted: 9 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Dietary zinc deficiency may lead to olfactory deficits, whose mechanism remains largely elusive. Olfactory ensheathing cells (OECs), a type of glial cells that support the function and neurogenesis in the olfactory bulb (OB), may play a pivotal role in the maintenance of the olfactory system. In the present study, we established a rat model of dietary zinc deficiency and found that severe zinc deficiency, but not marginal zinc deficiency, caused significantly reduced food intake, growth retardation, and apparent olfactory deficit in growing rats. We showed that severe zinc deficiency resulted in the loss of OECs in the olfactory nerve layer (ONL) of the olfactory bulb. In addition, we revealed that the number of TUNEL-positive cells increased markedly in the region, suggesting an involvement of apoptotic cell death in zinc deficiency-induced loss of OECs. Moreover, we found that treatment with zinc chelator N,N,N′N′,-tetrakis (2-pyridylmethyl)ethylenediamine (TPEN) triggered the apoptosis of in vitrocultured primary OECs. The apoptosis of OECs was correlated with significantly elevated expression of p53. Importantly, TUNEL and CCK-8 assays both demonstrated that treatment with p53 antagonist pifithrin-α (PFT-α) markedly attenuated TPEN-induced OEC apoptosis. These findings implicated that p53-triggered apoptosis of OECs might play an integral role in zinc deficiency-induced olfactory malfunction. Keywords Zinc deficiency . Olfactory deficit . Olfactory ensheathing cells . Apoptosis
Abbreviations OECs Olfactory ensheathing cells OB Olfactory bulb ppm Parts per million TPEN N,N,N′N′,-tetrakis (2-pyridylmethyl)ethylenediamine PFT-α Pifithrin-α NPCs Neural precursor cells SVZ Subventricular zone ROS Reactive oxidative species Zinc is an important trace element for the development and physiological maintenance of various human organs. Dietary Yu Jiang and Lingqi Gu contributed equally to this work. * Chunhua Wan [email protected] 1
Department of Nutrition and Food Hygiene, School of Public Health, Nantong University, No. 9, Seyuan Road, Nantong 226001, People’s Republic of China
2
Department of Pharmacy, Nantong Maternal and Child Health Hospital, 399 Century Avenue, Nantong 226018, Jiangsu, China
zinc deficiency causes neurological deficits and leads to behavioral abnormalities. For instance, prenatal and postnatal dietary zinc deficiency has been linked to the impairment of learning and memory capacities in adult rats (Halas et al. 1983; Halas et al. 1986). In spite of the difficulties in clinic diagnoses of zinc deficiency, accumulating evidence has indicated that zinc deficiency may contribute to lethargy, anxiety, anorexia, and immunological lesions (Krebs et al. 2014; Sandstead 2012). Moreover, zinc
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