Journal of Endocrinology and Reproduction

P. Sekar ¹, G. Vengatesh ¹, M. Kathiresh Kumar ¹, S. Balaji ¹, M. A. Akbarsha ², M. M. Aruldhas ³

Affiliations
1 Department of Endocrinology, Dr. ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, IN
2 Department of Animal Science, Bharathidasan University, Tiruchirappalli - 620 024, IN
3 Department of Endocrinology, Dr. ALM Post-Graduate Institute of Basic Medical Sciences, University of Madras Taramani Campus, Chennai - 600 113, IN

Abstract

Reproductive and embryonic toxicity of hexavalent chromium (CrVI) is known, and adult testis is one of its vulnerable targets. However, it is not known if gestational and lactational exposure to excess Cr affects development and functions of Leydig cells during postnatal life. It is hypothesized that gestational/lactational exposure to CrVI may affect Leydig cell development and differentiation and its functions during postnatal life extending into adulthood. Pregnant [gestational days 9 to 21] and lactating [postnatal days (PND) 1 to 21] rats were exposed to 50ppm and 100ppm CrVI (K₂Cr₂O₇) through drinking water, and testis was collected on PND 30, 60, 90 and 120, and subjected to light and transmission electron microscopic analysis. Serum testosterone and estradiol were determined adopting RIA. Histological evaluation of testes revealed hypertrophy and vacuolation of Leydig cells of CrVI-exposed rats; transmission electron micrographs (TEM) showed lipid accumulation, swollen mitochondria and disorganized smooth endoplasmic reticulum. Lactational exposure to CrVI led to decrease in the number of mitochondria and collapse of mitochondrial cristae. In general, the changes were obvious in PND 30 rats, and became less pronounced by PND 60 to become normal by PND 90. Serum testosterone and estradiol levels showed a general trend of opposite response to CrVI exposure. Gestational exposure to CrVI caused increase in testosterone level in prepuberal rats, but the trend was reversed by PND 60, and by PND 120 its level was more than in coeval controls. A similar trend was noticed in rats which had lactational exposure to CrVI but for a consistent increase in both steroids in PND 30 and PND 60 old rats which were exposed to 50ppm CrVI. By PND 90, testosterone remained elevated or normal, but by PND 120 its level was increased due to lactational exposure to CrVI. On the contrary, serum estradiol in these rats was low by PND 90 and became normal by PND 120. The findings partially support the hypothesis proposed and it is concluded that the fetal type Leydig cells are the major targets for the toxic effects of CrVI exposure during gestational and lactational periods where in lactational exposure may have a persistent effect leading to increased testosterone: estradiol ratio. Nevertheless, the effects of CrVI on testosterone and estradiol are reversible, as the adult type Leydig cells are unaffected.

Keywords

CrVI, Estradiol, Leydig Cells, Sertoli Cells, Testicular Toxicity, Testosterone.

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M. Michael Aruldhas ¹, N. Kalpana ¹, G. Vengatesh ¹, K. Sakhila Banu ², P. Govindarajulu ¹

Affiliations
1 Department of Endocrinology, Dr. ALM PG Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600113, IN
2 Ontogenie et Reproduction, CRBR, CHUL, 2705 Boul W Lauira, Laval University Stc Roy, que, GIV 4G2, CA

Abstract

Existing modes of diagnosis and therapy for medullary thyroid carcinoma (MTC) have limitations, informations on the genetics of familial medullary thyroid carcinoma (FMTC), a constituent of multiple endocrine neoplasia II (MEN II) syndrome may help to understand the etiology of the disease and to design gene therapy. Association between specific mutations in ret protooncogene to specific phenotypes of MEN II subjects provide vital line of due for the diagnosis of the disease. Screening of suspected/potent carriers of ret (rearranged during transformation) mutations will help to decide about the time and course of treatment. Gene therapy for MTC appears to be imminent and this review attempts to provide a comprehensive account of informations from more than hundred research articles published in this area.

Keywords

Calcitonin, Familial Medullary Thyrold Carcinoma, Gene Therapy, Immuno Therapy, Medullary Thyroid Carcinoma, Multiple Endocrine Neoplasia, Ret Protooncogene.

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A. M. J. Sashi ¹, N. S. Venkatesh ¹, P. Sekhar ¹, J. Anbalagan ¹, G. Vengatesh ¹, P. Govindarajulu ¹, M. M. Aruldhas ¹

Affiliations
1 Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai 600 113, IN

Abstract

Hypogonadism and male infertility associated with congenital hypothyroidism are two important reproductive health problems. Studies emanated from our laboratory and a few others have established thyroid hormone as an important regulator of testicular development, growth, structure and function. Existing literature are centering around the effect of neonatal, prepuberal and puberal onset hypothyroidism on the testis of adult rats.

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P. Sekhar ¹, S. Subramanian ², N. S. Venkatesh ², A. M. J. Sashi ², N. Kalpana ², J. Anbalagan ², G. Vengatesh ², P. Govindarajulu ², M. A. Akbarsha ³, M. M. Aruldhas ²

Affiliations
1 Post Graduate Department of Zoology, Voorhees College, Vellore-632001, IN
2 Department of Endocrinology, University of Madras, Dr. ALM Post Graduate Institute of Basic Medical Sciences, Taramani Campus, Chennai-600113, IN
3 Department of Animal Science, Bharathidasan University, Tiruchirappalli-620024, IN

Abstract

Heavy metals and chemicals are known to cause male infertility. Chromium, an occupational heavy metal pollutant is a wellknown carcinogen with toxic effect on skin, lung and kidney. A few early reports point out the reproductive toxicity of chromium in experimental animals. An extensive study conducted in our laboratory in adult rats and monkeys established that altered prooxidant - antioxidant balance leading to free radical toxicity in the testis as the mechanism underlying the reproductive toxicity of chromium.

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A. M. J. Sashi ¹, N. S. Venkatesh ¹, G. Vengatesh ¹, P. Sekhar ¹, J. Anbalagan ¹, N. Kala ¹, P. Govindarajulu ¹, M. A. Akbarsha ², M. M. Aruldhas ¹

Affiliations
1 Department of Endocrinology, Dr. ALM Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai-600113, IN
2 Department of Animal Science, Bharathidasan University, Tiruchirappalli-620024, IN

Abstract

Recent demonstration of thyroid hormone receptors (TR) in epididymis by our laboratory and that of Del Rio point out that epididymis may also be a target for the direct effect of T₃. Recent studies emanating from our laboratory have shown the importance of foetal-onset hypothyroidism on the growth, structure and function of the epididymis in adult rats. Since there are temporal difference in the foetal differentiation of hypothalamo-hypophyseal-testicular axis and the differentiation of testis and epididymis, it is hypothesized "Transient maternal hypothyroidism modifies specific cell types of the epididymis during pre-puberal, puberal and adult period in a temporal manner".

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