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Effects of methyl mercury on sperm oxygen consumption
Abstract:
Oxygen consumption and percent motile spermatozoa were determined for semen samples from healthy male monkeys Macaca fascicularis. Methyl mercury was added to the samples, in the oxygen measurement chamber, at a concentration of 9 p.p.m. for 15 min. and then increased to 15 p.p.m. for 15-30 min. Oxygen consumption and percent motility were determined during each period. Methyl mercury addition resulted in decreased sperm motility, but we did not detect any inhibition in the rate of oxygen consumption accompanying the decreased motility. On the contrary, the rate of oxygen consumption increased at 15 p.p.m. within 15 min., while the sperm motility was close to zero. Antimycin inhibited the increased rate of oxygen consumption demonstrating the mitochondrial source of this increased rate. Oligomycin also inhibited the increased rate of oxygen consumption due to methyl mercury, thus excluding the possibility of uncoupling of mitochondrial oxidative phosphorylation. Interference with mitochondrial energy production does not seem to be the primary mechanism of methyl mercury-induced decreased spermatozoal motility. Methyl mercury interference with the dynein/microtubule sliding assembly now seems to us to be a more tenable hypothesis.
Insights
Methyl mercury significantly reduces sperm motility in Macaca fascicularis monkeys. However, it does not inhibit oxygen consumption; instead, it increases it, suggesting energy production is not the primary target.
Area of Science:
- Reproductive Toxicology
- Environmental Health
- Spermatozoa Physiology
Background:
- Methyl mercury is a known environmental toxin with potential adverse effects on reproductive health.
- Spermatozoa motility is crucial for male fertility and is energy-dependent.
- Understanding the mechanisms of methyl mercury toxicity in sperm is important for assessing reproductive risks.
Purpose of the Study:
- To investigate the effects of methyl mercury on oxygen consumption and motility of Macaca fascicularis spermatozoa.
- To determine the primary mechanism by which methyl mercury impairs sperm function.
Main Methods:
- Semen samples from Macaca fascicularis were exposed to varying concentrations of methyl mercury (9-15 p.p.m.).
- Oxygen consumption and sperm motility were measured during methyl mercury exposure.
- The effects of antimycin and oligomycin on methyl mercury-induced changes were assessed to probe mitochondrial function.
Main Results:
- Methyl mercury exposure led to a significant decrease in sperm motility.
- Oxygen consumption rates increased with methyl mercury exposure, particularly at 15 p.p.m., when motility was near zero.
- Antimycin and oligomycin inhibited the increased oxygen consumption, confirming mitochondrial involvement but ruling out uncoupling of oxidative phosphorylation.
Conclusions:
- Methyl mercury's primary mechanism of action on sperm motility does not involve direct interference with mitochondrial energy production.
- The observed increase in oxygen consumption suggests a compensatory response or alternative metabolic pathway activation.
- Methyl mercury's interference with dynein/microtubule sliding assembly is a more plausible hypothesis for reduced sperm motility.