Goitrogenic/antithyroidal potential of moringa leaves (Moringa oleifera) and spinach (Spinacia oleracea) of Indian origin on thyroid status in male albino rats

Chiranjit Mondal,Amar Kumar Chandra

doi:10.1590/s2175-97902019000218005

Chiranjit Mondal, Amar Kumar Chandra

Open Access

https://doi.org/10.1590/s2175-97902019000218005

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Abstract

Moringa leaves and spinach used as vegetables containing cyanogens and polyphenols having suspected antithyroidal activity; however, detailed studies in this aspect found unavailable. Goitrogenic/antithyroid potentiality of those plant foods of Indian origin was evaluated. To explore the goitrogenic/antithyroid effect of those plant foods cyanogenic glucosides, glucosinolates, thiocyanate and polyphenol content were measured. These plant foods were fed with diet regularly to adult male albino rats for 30 and 60 days respectively, followed by evaluation of morphological and functional status of thyroid,as thyroid gland weight, the activity status of thyroid hormone synthesizing enzymes viz. TPO, Na+-K+-ATPase, deiodinase I, thyroid hormone profiles, thyroid histoarchitecture as well as urinary iodine and thiocyanate. In moringa leaves and spinach fed diet, there was a significant increase in urinary excretion of thiocyanate and iodine, enlargement of thyroid gland along with hypertrophy of thyroid follicles and altered in the activities of thyroid hormone synthesizing enzymes with concomitant changes of thyroid hormone profiles. Effects were more severe in moringa leaves treated group than that of spinach. Biochemical analysis moringa leaves and spinach reveal that those are rich sources of goitrogens and their prolonged consumption gradually developed a relative state of biochemical and morphological hypothyroidism.

Highlights

Iodine deficiency is well characterized as the main nutritional risk factor for thyroid dysfunction
Universal salt iodisation (USI) is recognised as the most promising and sustainable solution to combat the risk of iodine deficiency disorders (IDDs) at the country level (Global Report, 2009).The use of iodized salt has been introduced and still in practice in India for last few decades to minimise the rate of prevalence of IDDs, but the national programme has experienced major setbacks
Goitrogen containing foods are capable of altering thyroid function by interfering iodide uptake of thyroid tissue or interfering the organification of iodine or inhibiting the activity of thyroid peroxidase that catalyses the reactions for thyroid hormone synthesis (Gaitan, 1990).There are certain plant foods that have goitrogens in different concentrations found to exacerbate the goiter formation in the population having inadequate iodine intake and even in those with adequate iodine intake (Chandra et al, 2004)

Summary

Introduction

Iodine deficiency is well characterized as the main nutritional risk factor for thyroid dysfunction. Inadequate intake of iodine causes insufficient amount thyroid hormone production, which leads to adverse outcomes of health, termed as iodine deficiency disorders (IDDs) (Zimmermann, Jooste, Pandav, 2008). Iodine deficiency is a major global public health challenge. Universal salt iodisation (USI) is recognised as the most promising and sustainable solution to combat the risk of IDDs at the country level (Global Report, 2009).The use of iodized salt has been introduced and still in practice in India for last few decades to minimise the rate of prevalence of IDDs, but the national programme has experienced major setbacks. Regular consumption of plant foods containing goitrogens affect thyroid physiology and may lead to the development of endemic goitre, especially in iodine deficient environments (Delange et al, 1982). Goitrogen containing foods are capable of altering thyroid function by interfering iodide uptake of thyroid tissue or interfering the organification of iodine or inhibiting the activity of thyroid peroxidase that catalyses the reactions for thyroid hormone synthesis (Gaitan, 1990).There are certain plant foods that have goitrogens in different concentrations found to exacerbate the goiter formation in the population having inadequate iodine intake and even in those with adequate iodine intake (Chandra et al, 2004)

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