Physiological function of nickel as an essential trace nutrient for reproduction

Abstract

Physiological function of nickel as an essential nutrient for reproduction is discussed. Nickel deficiency induces abnormality in reproduction. In goats, nickel deficiency decreases the success rate of the first insemination and increases the abortion rate. In minipigs, nickel deficiency causes a retardation in pregnancy and delivery of offspring. In rats, nickel deficiency causes a decrease in epididymal sperm density, spermatozoa motility, epididymal transit time, and testicular sperm production rate, as well as weights of seminal vesicles and prostates. Since cyclic nucleotide-gated (CNG) cation channel subunits A3 and B1 distribute in the sperm flagellum, potentiation of CNG channels by Ni²⁺ may be responsible for reproductive abnormality induced by nickel deficiency. Since Ni²⁺ stabilizes the C3-convertase C3b-Bb complex in the alternative pathway of the complement system and seminal plasma contains a relatively high level of nickel, nickel may have a role in preventing male reproductive tract infection.