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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #116942


item Nielsen, Forrest - Frosty
item Uthus, Eric
item Yokoi, Katsuhiko

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/10/2000
Publication Date: 3/7/2001
Citation: Nielsen, F.H., Uthus, E.O., Yokoi, K. 2001. Dietary nickel deprivation decreases sperm motility and evokes hypertension in rats [abstract]. The Federation of American Societies for Experimental Biology Journal. 15:A972.

Interpretive Summary:

Technical Abstract: Nickel (Ni) alters cyclic nucleotide-activated cation channels via an interaction with cyclic GMP (Gordon, Neuron 14:857, 1995). To test the hypothesis that Ni has a biological role that affects the cyclic GMP signal transduction system, physiological functions involving cyclic GMP, i.e., sperm motility and blood pressure control of male weanling Sprague- Dawley rats (N = 15 - 16/ group) were determined after being fed a Ni- deficient basal diet (15 ng Ni/g) supplemented with 0 and 1 mg Ni/kg. After 5 weeks of feeding the experimental diets, N-nitro-L-arginine methyl ester (NAME, a nitric oxide synthase inhibitor) was given in the drinking water (0.5 g/L) daily to half of the animals in each group. Blood pressure was measured one week later. Three weeks after the NAME treatment began, epididymal sperm motility and density were measured. Nickel deprivation decreased sperm motility and density, and increased blood pressure. These results suggest that nickel is an essential nutrient that is physiologically important in functions involving the cyclic GMP signal transduction system.