Nickel deficiency diminishes sperm quantity and movement in rats

• Published in: Biological trace element research 2003, Vol.93 (1-3), p.141-153
• Main Authors: Yokoi, Katsuhiko, Uthus, Eric O, Nielsen, Forrest H
• Format: Article
• Language: English
• Subjects: animal reproduction; Animals; cyclic nucleotide-gated channels; deficiency diseases; Diet; dietary mineral supplements; Dietary Supplements; Drinking water; enzyme inhibitors; epididymis; Epididymis - cytology; Epididymis - drug effects; Epididymis - physiology; Experiments; Male; NG-Nitroarginine Methyl Ester - administration & dosage; NG-Nitroarginine Methyl Ester - pharmacology; Nickel; Nickel - administration & dosage; Nickel - deficiency; Nickel - pharmacology; Nitric oxide; nitric oxide synthase; nutrient deficiencies; Organ Size - drug effects; Physiology; prostate gland; Rats; Rats, Sprague-Dawley; Reproduction; Rodents; Sodium chloride; Sodium Chloride, Dietary - pharmacology; Sperm Count; sperm motility; Sperm Motility - drug effects; Sperm Motility - physiology; spermatozoa; Spermatozoa - cytology; Spermatozoa - drug effects; Spermatozoa - physiology; testes; weanlings
• ISSN: 1559-0720; 0163-4984; 1559-0720; 0163-4984
• DOI: 10.1385/bter:93:1-3:141

Early studies on nickel essentiality with rats and goats indicated that nickel deprivation impaired reproductive performance. Nickel also has been found to influence cyclic nucleotide gated channels (CNG); these types of channels are important in sperm physiology. Thus, two experiments were conducted to test the hypothesis that nickel deficiency affects sperm physiology in a manner consistent with nickel having an essential function related to CNG channel functions. The experiments were factorially arranged with four treatment groups of eight weanling rats in each. In experiment 1, the treatments were supplemental dietary nickel of 0 and 1 mg/kg and N(ω)-nitro-l-arginine methyl ester (l-NAME, a nitric oxide synthase inhibitor) added to the drinking water (50 mg/100 mL) the last 3 wk of an 8-wk experiment. In experment 2, the treatments were supplemental dietary nickel at 0 and 1 mg/kg and supplemental dietary sodium chloride (NaCl) at 0 and 80 g/kg. The NaCl and l-NAME variables were included to act as stressors affecting CNG channel activity. The basal diet contained per kilogram about 27 µg of nickel and 1 g of sodium. After 8 wk in experiment 1 and 16 wk 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. Excessive NaCl had no effect on sperm physiology; however, it decreased prostate gland weights. The findings support the hypothesis that nickel has an essential function that possibly could affect reproductive performance in higher animals, perhaps through affecting a CNG channel function.