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Dec 28, 2017 - endocrine- and neural-disrupting actions on the development of THs- brain axis. Thus, any insignificant alterations in the thyroid function.
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ISSN: 2161-1017

Endocrinology & Metabolic Syndrome

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Ahmed et al., Endocrinol Metab Syndr 2017, 6:6 DOI: 10.4172/2161-1017.1000281

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Maternal Anticancer Drugs and Fetal Neuroendocrine Dysfunction in Experimental Animals Ahmed RG* Division of Anatomy and Embryology, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt *Corresponding author: Ahmed RG, Division of Anatomy and Embryology, Zoology Department, Faculty of Science, Beni-Suef University, Beni-Suef, Egypt, Tel: 002-010-91471828; E-mail: [email protected] Received date: November 16, 2017; Accepted date: December 12, 2017; Published date: December 28, 2017 Copyright: © 2017 Ahmed RG. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Anti-Cancer Drugs Increase demand of gestational thyroid hormones (THs) is necessary for the fetal development [1-40]. Doxorubicin (DOX) is an anticancer drug that is used widely in treating leukemias, lymphomas, lung, breast, ovary and uterine cancers [41]. However, its injection during pregnancy initiated thyroid dysgenesis and disorganization [42,43], hypothalamic-pituitary-thyroid axis (HPTA) dysfunction [43,44], GH-resistance [45], growth retardation [46,47], and CNS damage in children or adults [48]. Furthermore, thyroid disorders in rats are commonly disturbed the inorganic phosphate (Pi) and Ca2+ homeostasis [49]. The impairment in the Ca2+-ATPase function was observed in the hypothyroid rat brain [50,51]. Also, the neonatal hypothyroidism can cause the following: (1) impair the synaptic transmission [52,53]; (2) disturb the Na+, K+ATPase activity [3,6]; (3) alter the kinetic properties of Na+, K+ATPase [54,55]; (4) diminish the metabolic and electrical activities [52,53,56]; and (5) delay the neuronal-oligodendrocyte functions [57]. In general, the deficiency in the rate of ATP synthesis [50,58,59] and in the rate of AMP-activated protein kinase (AMPK) [60] was decreased significantly in the hypothyroid state. This reduction can inhibit fatty acid oxidation [60] and impair the energy production [61]. On the other hand, my group reported that the activities of fetal ATPaseenzymes system (Na+, K+-ATPase, Ca2+-ATPase and Mg2+-ATPase) were decreased in cerebrum and cerebellum of maternal DOX group [33]. In parallel, DOX decreased ATP [62] and ATP/ADP ratio [62,63], inhibited Na+/K+ pump [64] and sarcoplasmic reticulum Ca2+ATPase [62], and increased apoptotic pathways [65]. Thus, DOX may act as endocrine- and neural-disrupting actions on the development of THsbrain axis. Thus, any insignificant alterations in the thyroid function during the development can cause brain damage [2,6,7,66]. Also, clinical studies displayed that maternal TH deficiency during the first trimester of pregnancy can affect the outcome of human neurodevelopment [67,68]. For these reasons, I recommend annual estimation for THs and growth rates for DOX-mothers and their neonates [33]. Obviously, investigations in this field are still in its beginnings, with numerous significant and challenging issues remaining to be addressed.

Conflict of Interest The author declares that no competing financial interests exist.

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Citation:

Ahmed RG (2017) Maternal Anticancer Drugs and Fetal Neuroendocrine Dysfunction in Experimental Animals. Endocrinol Metab Syndr 6: 281. doi:10.4172/2161-1017.1000281

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Ahmed RG (2017) Maternal Anticancer Drugs and Fetal Neuroendocrine Dysfunction in Experimental Animals. Endocrinol Metab Syndr 6: 281. doi:10.4172/2161-1017.1000281

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