Dataset Information

Dietary cholesterol-induced post-testicular infertility.

ABSTRACT: This work shows that an overload of dietary cholesterol causes complete infertility in dyslipidemic male mice (the Liver X Receptor-deficient mouse model). Infertility resulted from post-testicular defects affecting the fertilizing potential of spermatozoa. Spermatozoa of cholesterol-fed lxr-/- animals were found to be dramatically less viable and motile, and highly susceptible to undergo a premature acrosome reaction. We also provide evidence, that this lipid-induced infertility is associated with the accelerated appearance of a highly regionalized epididymal phenotype in segments 1 and 2 of the caput epididymidis that was otherwise only observed in aged LXR-deficient males. The epididymal epithelial phenotype is characterized by peritubular accumulation of cholesteryl ester lipid droplets in smooth muscle cells lining the epididymal duct, leading to their transdifferentiation into foam cells that eventually migrate through the duct wall, a situation that resembles the inflammatory atherosclerotic process. These findings establish the high level of susceptibility of epididymal sperm maturation to dietary cholesterol overload and could partly explain reproductive failures encountered by young dyslipidemic men as well as ageing males wishing to reproduce.

SUBMITTER: Ouvrier A

PROVIDER: S-EPMC3206870 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Dietary cholesterol-induced post-testicular infertility.

Ouvrier Aurélia A Alves Georges G Damon-Soubeyrand Christelle C Marceau Geoffroy G Cadet Rémi R Janny Laurent L Brugnon Florence F Kocer Ayhan A Pommier Aurélien A Lobaccaro Jean-Marc A JM Drevet Joël R JR Saez Fabrice F

PloS one 20111102 11

This work shows that an overload of dietary cholesterol causes complete infertility in dyslipidemic male mice (the Liver X Receptor-deficient mouse model). Infertility resulted from post-testicular defects affecting the fertilizing potential of spermatozoa. Spermatozoa of cholesterol-fed lxr-/- animals were found to be dramatically less viable and motile, and highly susceptible to undergo a premature acrosome reaction. We also provide evidence, that this lipid-induced infertility is associated w ...[more]

PMID: 22073227

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Project description:Binge drinking represents the major form of excessive alcohol (ethanol [EtOH]) consumption in the United States. Episodic (such as binge) drinking results in blood alcohol levels (BAL) of 18 to 80 mM and leads to alcohol-induced cerebral artery constriction (AICAC). AICAC was shown to arise from EtOH-induced inhibition of large-conductance, calcium/voltage-gated potassium (BK) channels in the vascular smooth muscle. Factors that modulate BK channel-mediated AICAC remain largely unknown.Male Sprague Dawley rats were placed on high-cholesterol (2% of cholesterol) diet for 18 to 23 weeks. Their littermates were placed on control iso-caloric diet. AICAC was evaluated both in vivo and in vitro, by means of pial arteriole diameter monitoring through a closed cranial window and diameter measurements of isolated, pressurized cerebral arteries. Cholesterol level in the cerebral artery tissue was manipulated by methyl-?-cyclodextrin to reverse dietary-induced accumulation of cholesterol. BK channel surface presence on the plasma membrane of cerebral artery myocytes was evaluated by immunofluorescence staining. BK channel function in pressurized cerebral artery was assessed using selective BK channel blocker paxilline.Within 5 minutes of 50 mM EtOH injection into carotid artery in vivo, arteriole diameter decreased by 20% in control group. Pial arteriole constriction was significantly reduced in rats on high-cholesterol diet, resulting in only 10% reduction in diameter. BAL in both groups, however, remained the same. Significant reduction in AICAC in group on high-cholesterol diet compared to control was also observed after middle cerebral artery dissection and in vitro pressurization at 60 mmHg, this reduction remaining after endothelium removal. Cholesterol level in de-endothelialized cerebral arteries was significantly increased in rats on high-cholesterol diet. Removal of excessive cholesterol content restored AICAC to the level observed in cerebral arteries of rats on normal diet. Immunofluorescence staining of BK channel-forming and accessory, smooth muscle-specific ?1 subunit in freshly isolated cerebral artery myocyte showed that high-cholesterol diet did not down-regulate surface presence of BK protein. However, paxilline-induced cerebral artery constriction was diminished in arteries from rats on high-cholesterol diet.Our data indicate that dietary cholesterol protects against AICAC. This protection is caused by cholesterol buildup in the arterial tissue and diminished function (but not surface presence) of EtOH target-BK channel.

Project description:The exposure to diesel exhaust emissions (DEE) contributes to negative health outcomes and premature mortality. At the same time, the health effects of the exposure to biodiesel exhaust emission are still in scientific debate. The aim of presented study was to investigate in an animal study the effects of exposure to DEE from two types of biodiesel fuels, 1st generation B7 biodiesel containing 7% of fatty acid methyl esters (FAME) or 2nd generation biodiesel (SHB20) containing 7% of FAME and 13% of hydrotreated vegetable oil (HVO), on the oxidative stress in testes and possible protective effects of dietary intervention with blackcurrant pomace (BC). Adult Fisher344/DuCrl rats were exposed by inhalation (6 h/day, 5 days/week for 4 weeks) to 2% of DEE from B7 or SHB20 fuel mixed with air. The animals from B7 (n = 14) and SHB20 (n = 14) groups subjected to filtered by a diesel particulate filter (DPF) or unfiltered DEE were maintained on standard feed. The rats from B7+BC (n = 12) or SHB20+BC (n = 12), exposed to DEE in the same way, were fed with feed supplemented containing 2% (m/m) of BC. The exposure to exhaust emissions from 1st and 2nd generation biodiesel resulted in induction of oxidative stress in the testes. Higher concentration of the oxidative stress markers thiobarbituric acid-reactive substances (TBARS), lipid hydroperoxides (LOOHs), 25-dihydroxycholesterols (25(OH)2Ch), and 7-ketocholesterol (7-KCh) level), as well as decreased level of antioxidant defense systems such as reduced glutathione (GSH), GSH/GSSG ratio, and increased level of oxidized glutathione (GSSG)) were found. Dietary intervention reduced the concentration of TBARS, 7-KCh, LOOHs, and the GSSG level, and elevated the GSH level in testes. In conclusion, DEE-induced oxidative stress in the testes was related to the biodiesel feedstock and the application of DPF. The SHB20 DEE without DPF technology exerted the most pronounced toxic effects. Dietary intervention with BC in rats exposed to DEE reduced oxidative stress in testes and improved antioxidative defense parameters, however the redox balance in the testes was not completely restored.

Dataset Information

Dietary cholesterol-induced post-testicular infertility.

Publications

Dietary cholesterol-induced post-testicular infertility.

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