OBJECTIVE: To define the mechanism(s) underlying an association between asthenozoospermia and elevated blood, seminal plasma, and testicular cadmium levels in infertile human males using a rat model of environmentally relevant cadmium exposures. SETTING: University medical center andrology research laboratory. ANIMAL(S): Male Wistar rats (n = 60), documented to be sensitive to the testicular effects of cadmium. INTERVENTION(S): Rats were given ad libitum access to water supplemented with 14% sucrose and 0 mg/L, 5 mg/L, 50 mg/L, or 100 mg/L cadmium for 1, 4, or 8 weeks beginning at puberty. MAIN OUTCOME MEASURE(S): Testicular cadmium levels were determined by atomic absorption, cauda epididymal sperm motility by visual inspection, and testicular gene expression by DNA microarray hybridization. RESULT(S): Chronic, low-dose cadmium exposures produced a time- and dose-dependent reduction in sperm motility. Transcription of genes regulated by calcium and expression of L-type voltage-dependent calcium channel mRNA splicing variants were altered by cadmium exposure. Expression of calcium binding proteins involved in modulation of sperm motility was unaffected. CONCLUSION(S): A causal relationship between elevated testicular cadmium and asthenozoospermia was identified. Aberrrant sperm motility was correlated with altered expression of L-type voltage-dependent calcium channel isoforms found on the sperm tail, which regulate calcium and cadmium influx.
OBJECTIVE: To define the mechanism(s) underlying an association between asthenozoospermia and elevated blood, seminal plasma, and testicular cadmium levels in infertile human males using a rat model of environmentally relevant cadmium exposures. SETTING: University medical center andrology research laboratory. ANIMAL(S): Male Wistar rats (n = 60), documented to be sensitive to the testicular effects of cadmium. INTERVENTION(S): Rats were given ad libitum access to water supplemented with 14% sucrose and 0 mg/L, 5 mg/L, 50 mg/L, or 100 mg/L cadmium for 1, 4, or 8 weeks beginning at puberty. MAIN OUTCOME MEASURE(S): Testicular cadmium levels were determined by atomic absorption, cauda epididymal sperm motility by visual inspection, and testicular gene expression by DNA microarray hybridization. RESULT(S): Chronic, low-dose cadmium exposures produced a time- and dose-dependent reduction in sperm motility. Transcription of genes regulated by calcium and expression of L-type voltage-dependent calcium channel mRNA splicing variants were altered by cadmium exposure. Expression of calcium binding proteins involved in modulation of sperm motility was unaffected. CONCLUSION(S): A causal relationship between elevated testicular cadmium and asthenozoospermia was identified. Aberrrant sperm motility was correlated with altered expression of L-type voltage-dependent calcium channel isoforms found on the sperm tail, which regulate calcium and cadmium influx.
Authors: Susan Benoff; Russ Hauser; Joel L Marmar; Ian R Hurley; Barbara Napolitano; Grace M Centola Journal: Mol Med Date: 2009 Jul-Aug Impact factor: 6.354
Authors: Samy M Eleawa; Mahmoud A Alkhateeb; Fahaid H Alhashem; Ismaeel Bin-Jaliah; Hussein F Sakr; Hesham M Elrefaey; Abbas O Elkarib; Riyad M Alessa; Mohammad A Haidara; Abdullah S Shatoor; Mohammad A Khalil Journal: J Reprod Dev Date: 2014-02-01 Impact factor: 2.214