Abstract
Monocrotophos (MCP) is an organophosphorus pesticide that is median-toxic to fish. MCP pesticide resulted in an increase of 17 beta estradiol following a decrease in testosterone in male goldfish (Carassius auratus). To fully understand the mechanism of MCP pesticide that causes the imbalance between male and female hormones, we determined the levels of plasma cholesterol, spermatic steroidogenic acute regulatory protein mRNA, steroidogenesis enzyme mRNA, plasma sex hormone synthesis intermediates, and effectual hormones in male goldfish exposed to MCP pesticide at nominal concentrations of 0.01, 0.10, and 1.00 mg/L for 21 days in a semi-static exposure system. The results indicated that MCP pesticide (a) led to decreased steroidogenic acute regulatory protein mRNA levels; (b) decreased mRNA levels of cholesterol side chain cleavage enzyme and cytochrome P450 17 alpha hydroxylase, which are steroidogenesis enzymes involved in androgen synthesis; and (c) increased cytochrome P450 aromatase mRNA levels, a steroidogenesis enzyme involved in the synthesis of effectual estrogen. The present study provides evidence that MCP pesticide affects synthesis and conversion of sex steroids through multiple targets in male goldfish.
Highlights
Monocrotophos (MCP, CAS number 6923-22-4) is an organophosphorus pesticide that is high-toxic to birds, median-toxic to fish, and listed as a UNEP Prior Informed Consent chemical
Effects on plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) levels were examined to determine whether a lack of substrates for sex hormone synthesis is responsible for inhibited T levels
TC, high-density lipoproteins (HDL)-C, and Low-density lipoproteins (LDL)-C levels were not influenced by MCP pesticide exposure (Fig. 2)
Summary
Monocrotophos (MCP, CAS number 6923-22-4) is an organophosphorus pesticide that is high-toxic to birds, median-toxic to fish, and listed as a UNEP Prior Informed Consent chemical. MCP pesticide might affect synthesis and conversion of sex hormones via a number of pathways, such as changing the contents of synthesis substrates or influencing gene expression and activities of steroidogenesis enzymes.
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