The possible mode of action of prostaglandins: XVI. A study to assess the local effect of prostaglandins E1, E2 OR F2α in the regulation of male fertility

Rej, S.K.; Chatterjee, A.

doi:10.1016/0161-4630(80)90055-5

Cited by 5 publications

(5 citation statements)

References 10 publications

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“…Prostaglandin E and prostaglandin F have been shown to affect sperm metabolism and functions (Breitbart et al 1995; Herrero et al 1997; Kelly & Critchley, 1997), and enhance the contractility of the smooth muscle layer surrounding the epididymal tubule (Hib & Oscar, 1978; Cosentino et al 1984). Intratesticular injection of prostaglandins (Rej & Chatterjee, 1980) or Silastic implants bearing indomethacin (Ratnasooriya & Wadsworth, 1987) have been shown to suppress fertility in rats by mechanisms not entirely known. Our present experiments demonstrated that among the prostanoids tested, only PGE 2 , and to a much lesser extent PGF 2α , stimulate electrogenic anion secretion (driving force for water secretion) by the epididymis.…”

Section: Discussionmentioning

confidence: 99%

Regulation of anion secretion by cyclo‐oxygenase and prostanoids in cultured epididymal epithelia from the rat

Wong

Chan

Leung

et al. 1999

The Journal of Physiology

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The role of cyclo‐oxygenase (COX) in the regulation of anion secretion (measured as short‐ circuit current, Isc) in cultured epididymal epithelia from immature rats was investigated. COX inhibitors attenuated the increase of anion secretion caused by bradykinin (LBK) but had no effect on that caused by PGE2, suggesting that prostaglandin synthesis mediates the secretory response of the tissues to LBK. The apparent IC50 values for indomethacin, piroxicam and L‐745,337 in inhibiting the LBK‐induced Isc were 0·14, 1·34 and 15·7 μM, respectively. This order of potency: indomethacin > piroxicam > L‐745,337 >> DFU suggests the involvement of the COX‐1 isozyme in the mediation of the secretory response to LBK. Among the COX products (prostaglandins, thromboxane and prostacyclins) tested, only PGE2 and, to a much lesser extent, PGF2α stimulated anion secretion by cultured rat epididymal epithelia. The effect of PGE2 was mimicked by 11‐deoxyl PGE1, a specific prostaglandin E (EP)2/4 receptor agonist, but not by sulprostone, a specific EP1/3 receptor agonist, indicating that cyclic AMP‐coupled EP2/4 receptors are involved in the LBK‐stimulated anion secretion. A reverse transcriptase‐polymerase chain reaction study detected the expression of COX‐1 and COX‐2 mRNA in intact rat epididymis and in cultured epididymal epithelia. The expression of COX‐1 mRNA was reduced by LBK by 44 %. Immunohistochemical studies demonstrated the presence of COX‐1 immunoreactivity in the basal cells of the intact rat epididymis. By comparision, COX‐2 immunoreactivity was detected in the apical pole of the principal cells. The role of COX in the formation of the epididymal microenvironment and the implication of long term administration of non‐steroidal anti‐inflammatory drugs (NSAIDs) on male fertility are discussed.

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Section: Discussionmentioning

confidence: 99%

Regulation of anion secretion by cyclo‐oxygenase and prostanoids in cultured epididymal epithelia from the rat

Wong

Chan

Leung

et al. 1999

The Journal of Physiology

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“…More recent studies on human sperm function have shown that addition of PGE-2 to human semen samples increased the motility and ovum-penetrating ability of the spermatozoa (Aitken & Kelly, 1985). While most of the above-cited data indicate that seminal PGs enhance male fertility, some animal studies have shown that intrascrotal or intratesticular deposition of high doses of PGEs or PGF-2ot induce temporary sterility in rats and rabbits, probably by impairment of spermatogenesis (Saksena, Lau & Chang, 1978;Saksena & Lau, 1979;Rej & Chatterjee, 1980). While most of the above-cited data indicate that seminal PGs enhance male fertility, some animal studies have shown that intrascrotal or intratesticular deposition of high doses of PGEs or PGF-2ot induce temporary sterility in rats and rabbits, probably by impairment of spermatogenesis (Saksena, Lau & Chang, 1978;Saksena & Lau, 1979;Rej & Chatterjee, 1980).…”

Section: Discussionmentioning

confidence: 99%

Effect of non-steroidal anti-inflammatory drugs on fertility of male rats

Löscher¹,

Blazaki²

1986

Reproduction

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In an attempt to study the influence of seminal prostaglandin reduction on male fertility, the effect of prolonged treatment with 4 non-steroidal anti-inflammatory drugs (acetylsalicylic acid, indomethacin, naproxen and phenylbutazone) on fertility was determined in male rats. Before the fertility experiments, the pharmacokinetics of the drugs were determined to find dosage regimens by which drug concentrations known as active from human anti-inflammatory therapy could be reached and maintained in the animals. Except for phenylbutazone, all drugs decreased prostaglandin E-2 level in seminal fluid by 80-90%, but only indomethacin reduced fertility significantly. The results suggest that reduction of prostaglandin synthesis in male rats does not affect fertility, which might be related to the very low seminal prostaglandin levels in rats compared to those in animals of other species.

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“…Interestingly intratesticular injection of 2.5 mg/kg of PGE l , or PGE 2 affects the capacity of fertilizing of epididymal spermatozoa in male rats. Instead, no effects on male rat fertility were reported for PGF 2α , despite suppressing the testis and epididymis weight [35]. Both PGs of the E series (PGE 1 and PGE 2 ) did not have any local effect on epididymal spermatozoa fertilizing capacity, despite reducing the weight of the injected testis due to blood flow restriction at the site of application.…”

Section: Findings From Animal Studiesmentioning

confidence: 84%

“…Both PGs of the E series (PGE 1 and PGE 2 ) did not have any local effect on epididymal spermatozoa fertilizing capacity, despite reducing the weight of the injected testis due to blood flow restriction at the site of application. Considering that PGs suppress steroidogenesis by lowering the plasma levels of androgens, the incapacity of PGs to affect the fertilizing capacity of spermatozoa in both injected and contralateral sides suggests that the androgen that has been available following the treatment schedule was enough to keep the fertilizing capacity of the epididymal spermatozoa despite of the PGs site of injection [35]. However, intratesticular injection of higher doses of PGs (2.5 mg/kg) adversely affected the fertilizing ability of spermatozoa, by affecting steroidogenesis in both the injected and contralateral control testes [35].…”

Section: Findings From Animal Studiesmentioning

confidence: 99%

“…Considering that PGs suppress steroidogenesis by lowering the plasma levels of androgens, the incapacity of PGs to affect the fertilizing capacity of spermatozoa in both injected and contralateral sides suggests that the androgen that has been available following the treatment schedule was enough to keep the fertilizing capacity of the epididymal spermatozoa despite of the PGs site of injection [35]. However, intratesticular injection of higher doses of PGs (2.5 mg/kg) adversely affected the fertilizing ability of spermatozoa, by affecting steroidogenesis in both the injected and contralateral control testes [35]. The short-term treatment of hamsters with PGF 2α , or PGE 1 had no effect on fertilizing capacity [36,37].…”

Section: Findings From Animal Studiesmentioning

confidence: 99%

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Arachidonic Acid Pathways and Male Fertility: A Systematic Review

Hoxha

Barbonetti

Zappacosta

2023

IJMS

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Arachidonic acid (AA) is a polyunsaturated fatty acid that is involved in male fertility. Human seminal fluid contains different prostaglandins: PGE (PGE1 and PGE2), PGF2α, and their specific 19-hydroxy derivatives, 18,19-dehydro derivatives of PGE1 and PGE2. The objective of this study is to synthesize the available literature of in vivo animal studies and human clinical trials on the association between the AA pathway and male fertility. PGE is significantly decreased in the semen of infertile men, suggesting the potential for exploitation of PGE agonists to improve male fertility. Indeed, ibuprofen can affect male fertility by promoting alterations in sperm function and standard semen parameters. The results showed that targeting the AA pathways could be an attractive strategy for the treatment of male fertility.

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The possible mode of action of prostaglandins: XVI. A study to assess the local effect of prostaglandins E1, E2 OR F2α in the regulation of male fertility

Cited by 5 publications

References 10 publications

Regulation of anion secretion by cyclo‐oxygenase and prostanoids in cultured epididymal epithelia from the rat

Regulation of anion secretion by cyclo‐oxygenase and prostanoids in cultured epididymal epithelia from the rat

Effect of non-steroidal anti-inflammatory drugs on fertility of male rats

Arachidonic Acid Pathways and Male Fertility: A Systematic Review

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