Heena Shirwalkar

Publications (2)5.49 Total impact

• Article: Exposure of adult rats to estradiol valerate induces ovarian cyst with early senescence of follicles.

  Heena Shirwalkar, Deepak N Modi, Anurupa Maitra
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  ABSTRACT: Environmental and therapeutic estrogens are known to play an important role in modulating the reproductive life and pubertal maturation in males as well as in females. Animal studies have shown that exogenously administered estrogen induces follicular cysts. However, the probable mechanisms underlying this abnormal ovarian development and its impact on steroidogenesis have been ill defined. The present study was therefore carried out to understand the ontogeny of ovarian pathology owing to adult estrogenisation. Regularly cycling female Holtzman rats were sacrificed at one week, two weeks, three weeks and four weeks after a subcutaneous administration of 2 mg of estradiol valerate (E(2)V). The effect of this supra-physiological estrogen on serum endocrine profiles, development of follicular cysts, follicular apoptosis and expression of markers of folliculogenesis viz., estrogen receptor (ER)-beta, inhibin A and progesterone receptor (PR) were studied. Results indicate a temporal augmentation of steroidogenesis, which was associated with induction of follicular cyst with theca cell hyperplasia and induction of apoptosis in the primary and secondary follicles of the ovaries. Immuno-histochemical localization showed an increase in inhibin A with a reduction in ER-beta and PR indicating early maturation, poor follicle growth and granulosa cell differentiation. Results indicate that exposure to exogenous estrogen in adulthood can have deleterious effects on the ovarian physiology and endocrinology which may ultimately lead to cystogenesis, loss of follicle pool and early senescence.
  Molecular and Cellular Endocrinology 07/2007; 272(1-2):22-37. · 4.19 Impact Factor
• Article: Congenital adrenal hyperplasia: biochemical and molecular perspectives.

  Anurupa Maitra, Heena Shirwalkar
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  ABSTRACT: Congenital adrenal hyperplasia is a disorder occurring in both sexes and is the commonest cause of ambiguous genitalia. It is a group of autosomal recessive disorders in which, on the basis of an enzyme defect the bulk of steroid hormone production by adrenal cortex shifts from corticosteroids to androgens. Autosomal recessive mutations in the CYP21, CYP17, CYP11B1 and 3betaHSD genes that encode steroidogenic enzymes, in addition to mutations in the gene encoding the intracellular cholesterol transport protein steroidogenic acute regulatory protein StAR can cause CAH. Each of the defects causes different biochemical consequences and clinical features. Deficiencies in 21 hydroxylase (21-OH) and 11beta-Hydroxylase (11beta-OH) are the two most frequent causes of CAH. All the biochemical defects impair cortisol secretion, resulting into compensatory hypersecretion of ACTH and consequent hyperplasia of the adrenal cortex. Research in recent years has clarified clinical, biochemical and genetic problems in diagnosis and treatment of the disorders. Expanding knowledge of the gene mutations associated with each of these disorders is providing valuable diagnostic tools in addition to the biochemical profile and phenotype. Genotyping is useful in selecting instances to provide genetic counseling and to clarify ambiguous cases.
  Indian journal of experimental biology 08/2003; 41(7):701-9. · 1.29 Impact Factor