Kazim R Chohan1, Shawky Z A Badawy. 1. Department of Pathology, State University of New York, Upstate Medical University, Syracuse, NY 13210, USA. chohank@upstate.edu
Abstract
OBJECTIVE: The growing consensus on the negative impact of cigarette smoking on fertility prompted us to compare the rate of sperm respiration in smokers and non-smokers. MATERIALS AND METHODS: Semen samples from 20 smokers and 58 non-smokers consulting at the andrology laboratory for fertility evaluation were used. Smoking was defined as consumption of at least a half a pack per day. A phosphorescence analyzer that measures O(2) concentration in sperm suspensions as function of time was used to determine the rate of respiration. In a sealed vial, the rate of sperm respiration (k) was defined as -d[O(2)]/dt; where [O(2)] was obtained from the phosphorescence decay rate of a palladium phosphor. [O(2)] in solutions containing sperm and glucose declined linearly with time, showing the kinetics of O(2) consumption was zero-order. Inhibition of O(2) consumption by cyanide confirmed the oxidations that occurred in the sperm mitochondrial respiratory chain. RESULTS: There were no differences (p > 0.28) between smokers and non-smokers for ejaculate volume, motility, concentration, normal morphology, viability and hypo-osmotic swelling test. The rate (mean + or - SD, in microM O(2)/min/10(8) sperm) of sperm mitochondrial O(2) consumption in the smokers was 0.96 + or - 0.58 and in the non-smokers 1.39 + or - 0.67 (p = 0.004). CONCLUSIONS: The rate of sperm respiration was significantly lower in smokers. This negative impact of cigarette smoking on sperm aerobic metabolism may, in part, explain the lower rate of fertility in smokers.
OBJECTIVE: The growing consensus on the negative impact of cigarette smoking on fertility prompted us to compare the rate of sperm respiration in smokers and non-smokers. MATERIALS AND METHODS: Semen samples from 20 smokers and 58 non-smokers consulting at the andrology laboratory for fertility evaluation were used. Smoking was defined as consumption of at least a half a pack per day. A phosphorescence analyzer that measures O(2) concentration in sperm suspensions as function of time was used to determine the rate of respiration. In a sealed vial, the rate of sperm respiration (k) was defined as -d[O(2)]/dt; where [O(2)] was obtained from the phosphorescence decay rate of a palladium phosphor. [O(2)] in solutions containing sperm and glucose declined linearly with time, showing the kinetics of O(2) consumption was zero-order. Inhibition of O(2) consumption by cyanide confirmed the oxidations that occurred in the sperm mitochondrial respiratory chain. RESULTS: There were no differences (p > 0.28) between smokers and non-smokers for ejaculate volume, motility, concentration, normal morphology, viability and hypo-osmotic swelling test. The rate (mean + or - SD, in microM O(2)/min/10(8) sperm) of sperm mitochondrial O(2) consumption in the smokers was 0.96 + or - 0.58 and in the non-smokers 1.39 + or - 0.67 (p = 0.004). CONCLUSIONS: The rate of sperm respiration was significantly lower in smokers. This negative impact of cigarette smoking on sperm aerobic metabolism may, in part, explain the lower rate of fertility in smokers.
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