Increased risk of eosinophilic esophagitis with poor environmental quality as measured by the Environmental Quality Index.

Geographic differences in eosinophilic esophagitis (EoE) prevalence suggest the possibility that environmental exposures contribute to EoE pathogenesis. We aimed to examine the association between environmental quality and risk of EoE, using the Environmental Quality Index (EQI), which provides quantification of environmental quality in five domains: air, land, water, built, and sociodemographic for all counties in the United States. To do this, we performed a case-control study in a large pathology database. EoE cases were defined by ≥15 eosinophils per high-power field with other pathologic diagnoses excluded; controls did not have EoE. The pathology data were geocoded and linked with the EQI by county of residence. Logistic regression was used to estimate odds ratio (OR and 95% confidence interval [CI]) of EoE with overall EQI and for each domain, after adjusting for sex, age, and proportion minority race or ethnicity at the county level (higher EQI score indicates worse environmental quality). Of 29,802 EoE cases and 593,329 controls analyzed, odds of EoE were highest in the worst quintile of EQI (OR 1.25; 95% CI: 1.04-1.50), which was largely explained by poor scores in the water domain (OR: 1.33; 1.17-1.50). Conversely, odds of EoE were reduced with higher scores in the air domain (OR: 0.87, 0.74-1.03) and land domain (OR 0.87; 0.76-0.99). Poor EQI, mostly reflected by poor water quality, was associated with increased odds of EoE, while poor air and land quality were inversely associated with EoE. Additional work to identify specific water pollutants that may have an etiologic role in EoE may be warranted.

Associations between gastric histopathology and the occurrence of colonic polyps.

AIM: Compromise of the gastric acid barrier may facilitate bacterial invasion of the lower intestinal tract and promote the development of colonic neoplasia. Our study aimed to test the associations between histopathological abnormalities of the upper and lower gastrointestinal tract in patients undergoing bidirectional endoscopy. METHOD: The Inform Diagnostics database is a national electronic repository of histopathological records of patients distributed throughout the USA. A case-control study of 302 061 patients, 163 168 of whom had colonic polyps, evaluated whether the occurrence of colonic polyps was influenced by the presence of the following gastro-oesophageal diagnoses: gastric Helicobacter pylori infection, gastric intestinal metaplasia, fundic gland polyps and gastric hyperplastic polyps. The influence of individual diagnoses on the occurrence of colonic polyps was expressed as odds ratios with their 95% confidence intervals. RESULTS: The odds ratio for tubular adenomas being associated with gastric H. pylori was 1.53 (1.49-1.58), with intestinal metaplasia 1.65 (1.59-1.71), with fundic gland polyps 1.49 (1.45-1.54) and with gastric hyperplastic polyps 1.85 (1.75-1.96). The odds ratio for sessile serrated polyps being associated with gastric H. pylori was 1.03 (0.96-1.10), with intestinal metaplasia 1.21 (1.13-1.30), with fundic gland polyps 1.79 (1.69-1.89) and with gastric hyperplastic polyps 1.52 (1.35-1.71. CONCLUSION: A diminished gastric acid barrier function, which occurs in various upper gastrointestinal diseases associated with lowered gastric acid output, may promote the development of colonic neoplasia.

Decreased risk for microscopic colitis and inflammatory bowel disease among patients with reflux disease.

AIM: Previous studies have found an increased risk for microscopic colitis (MC) associated with proton pump inhibitors. In patients with ulcerative colitis (UC) or Crohn's disease (CD), proton pump inhibitors have been associated with an increased risk for IBD flares and impaired outcomes. The aim of this study was to test the epidemiological associations between gastro-oesophageal reflux disease (GERD) and MC, UC or CD in a large database. METHOD: The Miraca Life Sciences Database is a national electronic repository of histopathological records of patients distributed throughout the entire USA. A case-control study evaluated whether the presence of Barrett's metaplasia, erosive oesophagitis on endoscopy or histological signs of reflux oesophagitis, clinical diagnosis of GERD or any GERD type affected the occurrence of MC, UC or CD among 228 506 subjects undergoing bidirectional endoscopy. Multivariate logistic regression analyses were used to calculate ORs and their 95% CI for the risk of MC, UC or CD associated with various types of GERD and were adjusted for age, sex and presence of Helicobacter pylori. RESULTS: The analysis revealed an inverse relationship between GERD and different types of inflammatory bowel disease. The inverse relationships applied similarly to MC (mean = 0.62, 95% CI: 0.58-0.66), UC (mean = 0.89, 95% CI: 0.81-0.97) and CD (mean = 0.76, 95% CI: 0.69-0.85). It also applied to different forms of GERD, with a trend towards more pronounced inverse relationships associated with Barrett's metaplasia or erosive oesophagitis than clinical diagnosis of GERD. CONCLUSION: Gastro-oesophageal reflux disease is inversely associated with all forms of inflammatory bowel disease, such as MC, UC, or CD.

The ethnic distribution of sessile serrated polyps in the United States is inversely associated with Helicobacter pylori prevalence.

AIM: Little is known about the epidemiology of sessile serrated polyps (SSP). Our study aimed to investigate the influence of Helicobacter pylori gastritis and patient demographic characteristics (age, gender, ethnicity) on the prevalence of SSP using a large national database of patients undergoing bi-directional endoscopy. METHOD: De-identified patient data were extracted from the Miraca Life Sciences electronic database of histopathological reports. Using multivariate logistic regression analysis, the influence of H. pylori gastritis and demographic characteristics on the occurrence of SSP were expressed as odds ratios (OR) with their 95% confidence intervals (CI). RESULTS: The total study population comprised 228 506 subjects, of whom 28 890 carried a diagnosis of H. pylori gastritis and 11 285 SSP. Age (OR 4.35, 95% CI: 3.82-4.96), female gender (0.92, 0.88-0.95) and H. pylori gastritis (0.94, 0.88-0.99) exerted the strongest influence on the occurrence of SSP. In comparison with the population comprising Caucasians and African Americans, SSP were less common among subjects of Hispanic (0.67, 0.62-0.73), East Asian (0.59, 0.50-0.69), Indian (0.43, 0.27-0.64) or Middle Eastern descent (0.61, 0.41-0.87). All these ethnic subgroups were also characterized by a higher prevalence of H. pylori than the comparison group. A low prevalence of H. pylori was significantly associated with a high prevalence of SSP (R2  = 0.82, P < 0.001). CONCLUSION: The prevalence of SSP within the United States is characterized by a marked ethnic variation. The inverse correlation between the prevalence of H. pylori and SSP suggests that gastric infection with H. pylori may be partly responsible for the observed ethnic distribution of SSP.

Demographic and socioeconomic influences on Helicobacter pylori gastritis and its pre-neoplastic lesions amongst US residents.

BACKGROUND: Gastric infection with Helicobacter pylori (Hp) can lead to chronic inactive gastritis, atrophy and intestinal metaplasia. AIMS: To investigate in a cross-sectional study these changes among different socioeconomic and ethnic groups within the USA. METHODS: We used the Miraca Life Sciences database, an electronic depository of clinicopathological records from patients distributed throughout the USA, to extract data from 487 587 patients who underwent oesophago-gastro-duodenoscopy with biopsy between 1/2008 and 12/2014. We then classified patients into ethnic and socioeconomic categories using previously validated algorithms, as well as ZIP code-based information derived from the 2011-2012 US Census. RESULTS: The prevalence of Hp increased significantly until the age-group 40-49, before it leveled off and started a gradual decrease. The prevalence of chronic inactive gastritis, atrophy, and intestinal metaplasia increased significantly with age. The prevalence of Hp, chronic inactive gastritis, intestinal metaplasia, and atrophy decreased significantly with the percentage of Whites per ZIP code. The prevalence of all four diagnoses also decreased significantly with rising levels of income or college education. Hp, chronic inactive gastritis, atrophy and intestinal metaplasia were more common among Hispanics and the influence of income or college education less pronounced than in the entire population. Hp, chronic inactive gastritis, atrophy, and intestinal metaplasia were also more common among East-Asians, Hp and atrophy decreasing with rising income but remaining unaffected by levels of college education. CONCLUSION: Ethnicity and socioeconomic factors influence the occurrence of Hp gastritis, and its progression to chronic inactive gastritis, atrophy or intestinal metaplasia.

Differences in the socio-economic distribution of inflammatory bowel disease and microscopic colitis.

AIM: Inflammatory bowel disease (IBD) and microscopic colitis are characterized by different geographical distributions across the USA. In this cross-sectional study we utilized demographic and socio-economic information associated with individual ZIP codes to further delineate the epidemiological characteristics of the two diseases. METHOD: A total of 813 057 patients who underwent colonoscopy between 2008 and 2014 were extracted from an electronic database of histopathology reports. The prevalence of patients with IBD or microscopic colitis was expressed as percentage of the population associated with specific demographic (age, sex, ethnicity) and socio-economic characteristics (population size, housing value, annual income, tertiary education). RESULTS: Both diseases were more common among subjects from ZIP codes with predominantly White residents and less common among subjects from ZIP codes with predominantly non-White residents such as Black, Hispanic and Asian. These ethnic variations were more pronounced in microscopic colitis than IBD. Markers of affluence, such as average residential house value and annual income, were positively associated with IBD and negatively with microscopic colitis. The prevalence of both diseases was positively correlated with tertiary education. CONCLUSION: The occurrence of both IBD and microscopic colitis is influenced by environmental risk factors. The differences in the demographic, ethnic and socio-economic distributions of the two diseases suggest that different sets of risk factors affect the two diseases and that their aetiology is unrelated.

The influence of Helicobacter pylori on the ethnic distribution of Barrett's metaplasia.

BACKGROUND: Environmental risk factors associated with ethnicity may contribute to the occurrence of Barrett's metaplasia. AIM: To investigate the interaction between ethnicity and Helicobacter pylori infection in the occurrence of Barrett's metaplasia among patients undergoing oesophago-gastro-duodenoscopy. METHODS: The Miraca Life Sciences Database is an electronic repository of histopathological patient records. A case-control study evaluated the influence of age, gender, ethnicity and histological diagnosis of H. pylori on the occurrence of Barrett's metaplasia. RESULTS: The total study population comprised 596 479 subjects, of whom 76 475 harboured a diagnosis of Barrett's metaplasia. Male sex, age and H. pylori infection in declining order exerted the strongest influence on the occurrence of BM. In comparison with the population comprising Caucasians and African Americans, Barrett's metaplasia was less common among subjects of African (OR = 0.09, 95% CI = 0.01-0.43), Middle Eastern (0.26, 0.20-0.34), East Asian (0.35, 0.31-0.40), Indian (0.39, 0.32-0.47), Hispanic (0.62, 0.59-0.64) or Jewish descent (0.50, 0.45-0.54), but more common among subjects of Northern European descent (1.14, 1.03-1.26). With the exception of Jews and Northern Europeans, all other ethnic subgroups were characterised by a higher prevalence of H. pylori than the comparison group. A low prevalence of H. pylori was significantly associated with a high prevalence of Barrett's metaplasia (R2 = 0.82, P < 0.001), as well as dysplasia or oesophageal adenocarcinoma (R2 = 0.81, P < 0.001). CONCLUSION: Our analysis reveals an inverse relationship between the prevalence of Barrett's metaplasia and H. pylori gastritis among different ethnic groups within the United States.

Oesophageal signet ring cell carcinoma as complication of gastro-oesophageal reflux disease.

BACKGROUND: Signet ring cell carcinoma occurs as a histological variant of oesophageal adenocarcinoma. AIM: In a cross-sectional study, to pursue the hypothesis that oesophageal signet ring cell cancers constitute a complication of gastro-oesophageal reflux disease. METHODS: In a large national database of histopathology records, we accumulated 91 802 patients with Barrett's oesophagus (BE), 2817 with oesophageal nonsignet ring adenocarcinoma (EAC) and 278 with oesophageal signet ring cell carcinoma (SRC). The three groups were compared with respect to their clinical and demographic characteristics, as well as socio-economic risk factors (associated with patients' place of residence). RESULTS: About 9% of all oesophageal adenocarcinomas harboured features of signet ring cell carcinoma. Patients with oesophageal adenocarcinoma and signet ring cell carcinoma were characterised by almost identical epidemiological patterns. Patients with either cancer type were slightly older than those with Barrett's oesophagus (EAC 68.0, SRC 66.7 vs. BE 63.7 years), and both showed a striking male predominance (EAC and SRC 85% vs. BE 67%). Both cancer types were associated with a similar set of alarm symptoms, such as dysphagia, pain and weight loss. The distribution by race (Whites vs. Blacks) and socio-economic parameters, such as levels of college education and family income, were similar among the three groups of patients. CONCLUSIONS: Signet ring cell carcinoma is a rare variant of oesophageal adenocarcinoma with similar epidemiological characteristics. The reasons why a minority of reflux patients progress to develop signet ring cell carcinoma, rather than the usual type of oesophageal adenocarcinoma, remain unknown.

Progesterone triggers a wave of increased free calcium during the human sperm acrosome reaction.

The mammalian sperm acrosome reaction (AR), an essential fertilization event, requires an influx of Ca2+. The Ca2+ increase occurring in the human sperm head during the AR initiated by progesterone, a putative in vivo AR initiator, was investigated using video-image analysis with fura-2, a fluorescent Ca2+ probe. Progesterone treatment of capacitated human sperm resulted in a wave-like increase in sperm head cytosolic [Ca2+]i that appears to increase fastest in a region near the equatorial segment and then spreads throughout the rest of the head. The progesterone-mediated Ca2+ increase in the sperm head was strongly inhibited and the wave eliminated by picrotoxin, a blocker of GABAA receptor/Cl- channels and an inhibitor of the progesterone-mediated Cl- efflux and progesterone-initiated AR of human sperm. These results are the first to detect a ligand-mediated Ca2+ wave in sperm and to suggest that Cl- efflux influences Ca2+ influx during the AR.

The human acrosome reaction is highly sensitive to inhibition by cyclodiene insecticides.

The mammalian sperm acrosome reaction (AR) is essential to fertilization. It can be initiated in vitro by progesterone, a putative physiological initiator that helps to activate sperm GABA(A) receptor/chloride channels and by glycine, a substitute for the egg zona pellucida, which activates sperm glycine receptor/chloride channels. Even at 1 nM (0.41 ng/ml or 0.41 ppb), chlordane and endosulfan, chlorinated cyclodiene blockers of insect neuronal GABA(A) receptor/chloride channels, strongly inhibited the AR initiated by progesterone or glycine. Inhibition of the latter was also seen at 0.1 nM chlordane and endosulfan, but neither cyclodiene inhibited either AR initiator at 0.01 nM. Inhibitory concentrations of these cyclodienes are well within the range detected in human and wildlife tissue and fluids as a result of environmental contamination.

Chloride efflux during the progesterone-initiated human sperm acrosome reaction is inhibited by lavendustin A, a tyrosine kinase inhibitor.

Previous studies showed that progesterone (P) can initiate the mammalian sperm acrosome reaction (AR) in vitro and that a sperm GABAA-like receptor/Cl- channel is involved in an essential Cl- efflux mediated by P during the AR. Here, we show that lavendustin A, a potent, specific inhibitor of tyrosine kinase activity, strongly inhibits the P-initiated human AR and the essential P-mediated Cl- efflux. Lavendustin B, a weak tyrosine kinase inhibitor, had no significant effect. These results suggest that, as part of AR initiation, P mediates tyrosine phosphorylation of the sperm GABAA- like receptor/Cl- channel.

Progesterone-mediated efflux of cytosolic chloride during the human sperm acrosome reaction.

Progesterone is capable of initiating the mammalian sperm acrosome reaction in vitro and is a putative initiator of this essential fertilization event in vivo. Our previous work has suggested that progesterone initiates the human sperm acrosome reaction, at least in part, by activating a unique steroid receptor/Cl- channel resembling a gamma-aminobutyric acidA receptor/Cl- channel (gamma-aminobutyric acidA-like receptor/Cl- channel). Here, the fluorescent intracellular Cl- probe, 6-methoxy-N-ethylquinolinium, was used to detect qualitative changes in sperm cytosolic Cl-. We demonstrate that progesterone can mediate a rapid transient decrease of human sperm cytosolic Cl- inhibitable by the gamma-aminobutyric acidA receptor/Cl- channel antagonists picrotoxin and (+)-bicuculline (which also inhibit the acrosome reaction). These results support the involvement of a gamma-aminobutyric acidA-like receptor/Cl- channel in the P-mediated human acrosome reaction and are the first to demonstrate that a rapid Cl- efflux plays a role in that event.

Progesterone initiation of the human sperm acrosome reaction: the obligatory increase in intracellular calcium is independent of the chloride requirement.

The progesterone-initiated human sperm acrosome reaction (AR) requires a rise in intracellular Ca2+ ([Ca2+]i), extracellular Cl- and apparently increased Cl- flux through a unique steroid receptor/Cl- channel resembling but not identical to a GABA(A)/Cl- channel complex. The present study uses fura-2 loaded human sperm, GABA(A)/Cl- channel blockers (picrotoxin and pregnenolone sulfate) and Cl(-)-containing and Cl(-)-deficient media to determine whether the progesterone-mediated increase in [Ca2+]i is dependent on the Cl- requirement. There was no significant difference between the progesterone-mediated increases of [Ca2+]i obtained in Cl(-)-containing and Cl(-)-deficient media. Picrotoxin did not significantly inhibit the progesterone-mediated increase in [Ca2+]i, and pregnenolone sulfate increased [Ca2+]i to the same extent as progesterone. These results strongly suggest that the increase in [Ca2+]i essential to the AR is independent of the AR Cl- requirement and could be explained by the existence of two different sperm plasma membrane progesterone receptors.

Initiation of the human sperm acrosome reaction by thapsigargin.

Previous studies have established that the mammalian sperm acrosome reaction (AR) is dependent upon an influx of extracellular Ca2+, but the involvement of a mobilizable store of intracellular Ca2+ has not been shown. In many other cells, the endoplasmic reticulum is the site of such a Ca(2+)-store. Here, we show that thapsigargin, a highly specific inhibitor of the endoplasmic reticulum Ca(2+)-ATPase Ca(2+)-pump (and thus a mobilizer of intracellular Ca2+) in other cells, can initiate the AR in capacitated human sperm. Thapsigargin at concentrations from 50-500 nM significantly increased the AR to the same extent when incubated with capacitated sperm for 1 min (assayed by indirect immunofluorescence). Transmission electron microscopy confirmed the occurrence of normal morphology in the AR initiated by thapsigargin. Thapsigargin (200 nM) did not initiate the AR in noncapacitated sperm. Initiation of the AR by thapsigargin apparently requires an influx of Ca2+ since 1 min preincubation with the calcium channel blockers La3+ (250 microM) or Ni2+ (250 microM) prior to addition of thapsigargin completely inhibits AR-initiation. Mobilization of an intracellular Ca(2+)-store by thapsigargin in capacitated human sperm may lead to an influx of extracellular Ca2+ and subsequently the AR. Putative sites for thapsigargin-sensitive intracellular Ca(2+)-stores in human sperm include the cytoplasmic droplet, the sperm nucleus and the acrosome.

Effects of polyamine biosynthesis inhibitors on the progesterone-initiated increase in intracellular free Ca2+ and acrosome reactions in human sperm.

This laboratory has previously reported that progesterone can initiate a rapid transient increase in the concentration of intracellular free Ca2+ ([Ca2+]i) and an increase in a Ca(2+)-requiring exocytotic event, the acrosome reaction (AR) in human sperm. Rapid increases in Ca2+ fluxes of some mammalian cells caused by another steroid, testosterone, require polyamine biosynthesis. Herein, we tested two polyamine biosynthesis suicide inhibitors for their effects on the progesterone-initiated increase in [Ca2+]i and AR in capacitated human sperm in vitro: DL-alpha-(difluoromethyl)ornithine hydrochloride (DFMO), an inhibitor of putrescine synthesis by ornithine decarboxylase and (5'[[(Z)-4-amino-2-butenyl]methylamino]-5'-deoxyadenosine (MDL 73811), an inhibitor of S-adenosylmethionine decarboxylase (required for spermidine and spermine synthesis). Sperm were capacitated in vitro and preincubated 10 min with 4.9 mM DFMO or 9.8 microM MDL 73811 with or without various polyamines (245 microM). Progesterone (3.09 microM final concentration) or progesterone solvent (ethanol, 0.1% final concentration) was then added, sperm fixed 1 min after additions and AR assayed by indirect immunofluorescence or with fluorescein-labeled Con A lectin. DFMO strongly inhibited the AR, but putrescine (product of ornithine decarboxylase and precursor of spermidine and spermine) reversed that inhibition. Preincubation for 25 min with DMFO + spermidine also reversed DFMO inhibition. MDL 73811 inhibited the progesterone-initiated AR, and a 10 min preincubation with spermidine, but not putrescine or spermine, reversed that inhibition. Preincubations with putrescine alone or with spermidine alone followed by addition of the progesterone solvent did not initiate the AR, and such preincubations followed by progesterone addition did not increase the AR more than progesterone alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Progesterone acts at the plasma membrane of human sperm.

There has been increasing interest in the relationship between rapid effects of steroids and steroid-plasma membrane interaction. This laboratory has previously reported that progesterone increases human sperm cytosolic free calcium ([Ca2+]i) and thereby initiates the human sperm acrosome reaction (AR) in less than 1 min. Herein, to test whether progesterone acts at the sperm plasma membrane, progesterone 3-(O-carboxymethyl)oxime: bovine serum albumin (BSA) conjugate (free of unconjugated progesterone) was added to capacitated human sperm. Fura-2 assays were used to detect less than 1 min changes in [Ca2+]i, and indirect immunofluorescence was used to assay the AR occurring 1 min after stimulus addition. The conjugate increased [Ca2+]i and the AR (though less than did unconjugated progesterone). Enzyme immunoassays demonstrated that the concentrations of unconjugated progesterone in conjugate-treated sperm suspensions did not increase over those of control suspensions. Since the progesterone: BSA conjugate presumably does not cross the sperm plasma membrane, progesterone must act at that membrane to increase [Ca2+]i and the AR.

Zona pellucida-induced acrosome reaction in boar sperm.

Induction of the acrosome reaction in boar sperm by the zona pellucida (ZP) was investigated. A modified cytochemical staining method for measuring the acrosome reaction in boar sperm gave equivalent results to those obtained with transmission electron microscopy. Isolated heat-solubilized ZP effectively induced the acrosome reaction in boar sperm at a concentration of 25 micrograms/ml. Electrophoretically purified ZP components were also tested for acrosome reaction-inducing activity; both the 55,000 and 90,000 components of the ZP were effective. The carbohydrate moiety of the 55,000 component was necessary for activity because the polypeptides derived by chemical deglycosylation of the two glycoproteins did not induce the acrosome reaction.

Glycosaminoglycans stimulate the acrosome reaction of previously capacitated hamster sperm.

The glycosaminoglycans (GAGs) hyaluronic acid and heparin were added (10 micrograms and 100 micrograms/ml to golden hamster sperm suspensions previously incubated for 4.5 h under capacitating conditions. After additions, sperm were incubated for 5-15 min and acrosome reactions (AR) assayed in motile sperm by phase contrast microscopy. Hyaluronic acid and heparin significantly stimulated AR over control levels. Hyaluronic acid did not stimulate AR 15 min after addition to sperm previously incubated for only 2.5 h. Pre-incubation of hyaluronic acid with streptomyces hyaluronidase destroyed the ability of that GAG to stimulate the AR. These results indicate that GAGs (at least one of which, hyaluronic acid, is present in the oocyte cumulus oophorous) can rapidly stimulate the acrosome reaction in motile previously capacitated hamster sperm.

The effects of products and inhibitors of arachidonic acid metabolism on the hamster sperm acrosome reaction.

The mammalian sperm acrosome reaction (AR) is a fusion and fenestration of sperm head membranes which is essential for fertilization. Our earlier work demonstrated that arachidonic acid could stimulate the AR 15 min after addition to hamster sperm capacitated by incubation for 4.5 h. The present study was undertaken to determine whether inhibitors of arachidonic acid metabolism could affect the stimulation of the AR by arachidonic acid and whether products of its metabolism could stimulate the AR. Phenidone or nordihydroguaiaretic acid, inhibitors of both the cyclo-oxygenase and lipoxygenase pathways of arachidonic acid metabolism, and docosahexaenoic acid, a cyclo-oxygenase pathway inhibitor, inhibited the AR induced by arachidonic acid. PGE2, a product of the cyclo-oxygenase pathway of arachidonic acid metabolism and 5- or 12-hydroxyeicosatetraenoic acid (HETEs) products of the lipoxygenase pathway, stimulated the AR when added to sperm capacitated by incubation for 4.5 h. Prostaglandins not derived from arachidonic were also tested: PGE1 stimulated the AR, but PGF1 alpha and PGA2 did not. We suggest that arachidonic acid metabolites produced by the sperm and by the female reproductive tract are important for the mammalian sperm AR.

Stimulation of an exocytotic event, the hamster sperm acrosome reaction, by cis-unsaturated fatty acids.

The cis-unsaturated fatty acids oleic, arachidonic and cis-vaccenic stimulated the hamster sperm acrosome reaction in vitro (an exocytotic event which occurs in the sperm head and which is essential for fertilization). The trans-isomers of oleic and vaccenic acids did not stimulate the acrosome reaction, nor did the cis-unsaturated fatty acids petroselenic and docosahexaenoic or the saturated fatty acids lauric, myristic or stearic. This is the first report of a stimulatory effect of cis-unsaturated fatty acids on an exocytic event in an intact viable cell.