|Nielsen, Forrest - Frosty|
Submitted to: Biological Trace Element Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/10/2002
Publication Date: 6/1/2003
Citation: Yokoi, K., Uthus, E.O., Nielsen, F.H. 2003. Nickel deficiency diminishes sperm quantity and movement in rats. Biological Trace Element Research 93(1):141-154. Interpretive Summary: Early studies on nickel essentiality with rats and goats indicated that nickel deficiency impaired reproductive performance. Nickel also has been found to influence a system in cells that gives them signals to perform certain functions for normal vision, smell, and sperm physiology; this system is called cyclic nucleotide gated channels. Thus, two experiments were conducted with rats to find out whether nickel deficiency affects sperm physiology in a manner indicating that nickel is essential for some cyclic nucleotide gated channel functions, which ultimately could affect reproductive performance. In these experiments, rats were fed deficient and adequate amounts of nickel in the presence of stressors of cyclic nucleotide gated channel activity. The stressors were L-NAME in drinking water, and high dietary salt. L-NAME inhibits the activity of nitric oxide synthase, an enzyme that makes the molecule nitric oxide which stimulates cyclic nucleotide gated channel activity. High dietary salt increases atrial natriuretic peptide which increases the need for cyclic nucleotide gated channel activity. Nickel deficiency decreased spermatozoa motility and density in a reproductive organ (epididymis) in males and decreased testes sperm production rate. The changes were similar to those induced by L-NAME and were exacerbated by excessive dietary salt. Thus, the findings indicate that nickel has an essential function involving cyclic nucleotide gated channels which affect reproductive performance in higher animals, and thus possibly humans.
Technical Abstract: Early studies on nickel essentiality with rats and goats indicated that nickel deficiency impaired reproductive performance. Nickel also has been found to influence cyclic nucleotide gated (CNG) channels; these channels are important in sperm physiology. Thus, two experiments were conducted that were factorially arranged with 4 treatment groups of 8 weanling rats in each. In experiment 1, the treatments were supplemental dietary nickel at 0 and 1 mg/kg and N(G)-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase inhibitor) added to the drinking water (50 mg/mL) the last 3 weeks of an 8-week experiment. In experiment 2, the treatments were supplemental dietary nickel at 0 and 1 mg/kg and supplemental dietary sodium chloride (NaCl) 0 and at 80 g/kg. The NaCl and L-NAME variables were included to act as stressors affecting CNG channel activity. The basal diet contained per kg about 27 ug of nickel and 1 g of sodium. After 8 weeks in experiment 1 and 16 weeks in experiment 2, urine while fasting and testes and epididymis in both experiments, and seminal vesicles and prostates in experiment 2, were harvested for analysis. Nickel deprivation significantly decreased spermatozoa motility and density in the epididymides, epididymal transit time of spermatozoa, and testes sperm production rate. Nickel deficiency also significantly decreased the weights of the seminal vesicles and prostate glands. Animals treated with L-NAME had reduced sperm counts in the epididymis. Excessive NaCl had no effect on sperm physiology; however, it exacerbated changes induced by nickel deprivation. Excessive NaCl also decreased prostate gland weights. The findings support the hypothesis that nickel has an essential function involving CNG channels nimals.