Effects of subchronic exposure to waterborne cadmium on H-P-I axis hormones and related genes in rare minnows (Gobiocypris rarus)

Comp Biochem Physiol C Toxicol Pharmacol. 2017 Nov:202:1-11. doi: 10.1016/j.cbpc.2017.07.002. Epub 2017 Jul 22.

Abstract

The H (hypothalamic)-P (pituitary)-I (interrenal) axis is critical in the stress response and other activities of fish. To further investigate cadmium (Cd) toxicity on the H-P-I axis and to identify its potential regulatory genes in fish, the adult female rare minnows (Gobiocypris rarus) were exposed to subchronic (5weeks) levels of waterborne Cd in the present study. This kind of treatment caused dose-dependent decline in fish growth, with significance in the high dose group (100μg/L). Correspondingly, low dose (5-50μg/L) waterborne Cd disrupted the endocrine system of H-P-I axis just at the secretion level, while high dose Cd disrupted both the secretion and synthesis of cortisol and its downstream signals in rare minnows, revealed by the significantly upregulation and positive correlation of corticosteroidogenic genes including MC2R, StAR, CYP11A1, and CYP11B1 in the kidney (including the interrenal tissue) (P<0.05), and the significant alteration of Glcci1, Hsp90AA and Hsp90AB in the hepatopancreas, gill and intestine as well (P<0.05). The expression of Glcci1 was significantly decreased in hepatopancreas, gill and intestine of tested fish following treatment, and its positive correlation with GR (Glucocorticoid receptor) suggested its potential regulation on the cortisol and/or H-P-I axis in fish. The expression of FKBP5 in the intestine was positively and significantly correlated with that of Hsp90AA (P<0.05), and the Hsp90AB transcript in the hepatopancreas was positively correlated with that of Hsp90AA (P<0.05), which indicated that Hsp90AA and Hsp90AB were more likely to serve as cofactors of GR and FKBP5 in response to Cd exposure.

Keywords: FKBP5; Glcci1; Glucocorticoid receptor; H-P-I axis; Hsp90AA; Hsp90AB.

MeSH terms

  • Adrenocorticotropic Hormone / genetics
  • Adrenocorticotropic Hormone / metabolism
  • Animals
  • Cadmium Chloride / administration & dosage
  • Cadmium Chloride / toxicity*
  • Corticotropin-Releasing Hormone / genetics
  • Corticotropin-Releasing Hormone / metabolism
  • Cyprinidae / physiology*
  • Drug Administration Schedule
  • Female
  • Gene Expression Regulation / drug effects
  • Hydrocortisone / genetics
  • Hydrocortisone / metabolism
  • Hypothalamo-Hypophyseal System / drug effects*
  • Hypothalamo-Hypophyseal System / physiology
  • Interrenal Gland / drug effects*
  • Interrenal Gland / physiology
  • Melanocyte-Stimulating Hormones / genetics
  • Melanocyte-Stimulating Hormones / metabolism
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Tacrolimus Binding Proteins / genetics
  • Tacrolimus Binding Proteins / metabolism
  • Water Pollutants, Chemical / toxicity

Substances

  • RNA, Messenger
  • Water Pollutants, Chemical
  • Adrenocorticotropic Hormone
  • Melanocyte-Stimulating Hormones
  • Corticotropin-Releasing Hormone
  • Tacrolimus Binding Proteins
  • Cadmium Chloride
  • Hydrocortisone