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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 #130562


item Uthus, Eric
item Nielsen, Forrest - Frosty

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 2/1/2002
Publication Date: 5/5/2002
Citation: Yokoi, K., Uthus, E.O., Nielsen, F.H. 2002. The essential role of nickel affects physiological functions regulated by the cyclic-GMP transduction system [abstract]. Presented at the 7th International Symposium on Metal Ions in Biology and Medicine, St. Petersburg, Russia, May 5-9, 2002.

Interpretive Summary:

Technical Abstract: Two experiments were conducted with the objective of demonstrating that nickel (Ni)deprivation affects rats in a manner to support the hypothesis that Ni has an essential role involving the cGMP signal transduction system. Two stressors of systems in which cyclic nucleotide-gated (CNG) channels are important were used as treatment variables in addition to Ni; these were N-nitro-L-arginine methyl ester (L-NAME)supplementation and high dietary sodium chloride (NaCl). In experiment 1, rats (15-16/group) were fed a Ni-deficient basal diet (27 ng Ni/g) supplemented with 0 and 1 ug Ni/g. After 5 weeks of feeding the experimental diets, L-NAME was added to the drinking water (0.5 g/L) provided to half of the rats in each group. Blood pressure was measured one week later. Epididymal sperm motility and density were measured three weeks later. In experiment 2, the treatments (8 rats/treatment) were supplements to the basal diet (27 ng Ni and 1 mg NaCl/g) of 0 and 1 ug Ni/g and 0 and 80 mg NaCl/g for 16 weeks. Nickel deprivation increased blood pressure; decreased spermatozoa motility and density in the epididymides, epididymal transit time of spermatozoa, and testes sperm production rate; and induced macroscopic and microscopic kidney damage that resulted in hematuria and microalbuminuria. High NaCl exacerbated changes induced by Ni deprivation. The changes in blood pressure and sperm density caused by Ni deprivation were similar to those induced by L-NAME. Because L-NAME is a stressor of nitric oxide (NO) metabolism and excessive NaCl is a stressor of atrial natriuretic peptide (ANP) need, the changes suggest that Ni deficiency is detrimental to the ANP-cGMP and NO-cGMP signal transduction systems, and support the hypothesis that Ni has an essential function involving CNG channels.