[56] Physical chemistry, stability, and handling of prostaglandins E2, F2α, D2, and I2: A critical summary

Stehle, Randall G.

doi:10.1016/0076-6879(82)86216-2

Cited by 58 publications

(29 citation statements)

References 27 publications

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“…Thereafter, cells were stored at room temperature under sterile conditions and phytoprostane accumulation was monitored. As shown in Figure 4A, E 1 -phytoprostane (PPE 1 ) levels remained constant for at least 8 h. Thereafter, a more than 40-fold increase of PPE 1 levels was observed, reaching high levels after 20 h. Both regioisomers remained at this level (about 800 ng/g of dry weight) for at least 28 h. Since E-ring containing compounds such as PPE 1 are relatively stable in the physiological pH range, (Stehle, 1982) nonenzymatic degradation to PPA 1 /PPB 1 is a slow process leading to a delayed accumulation and low levels of these cyclopentenones (Fig. 4B).…”

Section: Delayed Formation Of Phytoprostanes In Metabolically Inactivmentioning

confidence: 83%

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

et al. 2005

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Phytoprostanes are prostaglandin/jasmonate-like products of nonenzymatic lipid peroxidation that not only occur ubiquitously in healthy plants but also increase in response to oxidative stress. In this work, we show that the two naturally occurring B 1 -phytoprostanes (PPB 1 ) regioisomers I and II (each comprising two enantiomers) are short-lived stress metabolites that display a broad spectrum of biological activities. Gene expression analysis of Arabidopsis (Arabidopsis thaliana) cell cultures treated with PPB 1 -I or -II revealed that both regioisomers triggered a massive detoxification and defense response. Interestingly, expression of several glutathione S-transferases, glycosyl transferases, and putative ATP-binding cassette transporters was found to be increased by one or both PPB 1 regioisomers, and hence, may enhance the plant's capacity to inactivate and sequester reactive products of lipid peroxidation. Moreover, pretreatment of tobacco (Nicotiana tabacum) suspension cells with PPB 1 considerably prevented cell death caused by severe CuSO 4 poisoning. Several Arabidopsis genes induced by PPB 1 , such as those coding for adenylylsulfate reductase, tryptophan synthase b-chain, and PAD3 pointed to an activation of the camalexin biosynthesis pathway that indeed led to the accumulation of camalexin in PPB 1 treated leaves of Arabidopsis. Stimulation of secondary metabolism appears to be a common plant reaction in response to PPB 1 . In three different plant species, PPB 1 -II induced a concentration dependent accumulation of phytoalexins that was comparable to that induced by methyl jasmonate. PPB 1 -I was much weaker active or almost inactive. No differences were found between the enantiomers of each regioisomer. Thus, results suggest that PPB 1 represent stress signals that improve plants capacity to cope better with a variety of stresses.Phytoprostanes belong to a novel family of plant effectors that are formed nonenzymatically by a free radical catalyzed biochemical mechanism from a-linolenic acid. Via an identical nonenzymatic mechanism, isoprostanes (isomers of prostaglandins) are formed in animals from arachidonic acid. Nomenclature used to name different phytoprostane classes conforms with the general isoprostane/prostaglandin terminology . Due to the nonenzymatic formation of phytoprostanes, two racemic regioisomers (type I and II) of each class can be generated. One pathway leads to the formation of B 1 -phytoprostanes (PPB 1 ; Fig. 1) that are chemically stable end products of lipid peroxidation. In animals, isoprostanes are not only extremely reliable markers of oxidative stress but also display potent (prostaglandin-) receptor-mediated biological activities in the nanomolar concentration range (Cracowski et al., 2002). Therefore, it is postulated that isoprostanes represent mediators of oxidant injury in animals.In plants, several classes of phytoprostanes are constitutively present, and, notably, their levels increase in a variety of conditions associated with enhanced free radical generatio...

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Section: Delayed Formation Of Phytoprostanes In Metabolically Inactivmentioning

confidence: 83%

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

et al. 2005

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“…While both these reactive intermediates are substrates for further enzymatic processing, chemically stable products can result from acid catalyzed hydrolysis. An additional biologically active eicosanoid, also chemically reactive, is PGI 2 which at pH 7.4 has a half-life of 3-4 min at 37°C [12]. The instability of these three reactive compounds at physiological pH has made their separation and direct measurement by physical chemical methods quite problematic.…”

mentioning

confidence: 99%

Mass spectrometric analysis of leukotriene A₄ and other chemically reactive metabolites of arachidonic acid

Dickinson

Murphy

2002

J. Am. Soc. Mass Spectrom.

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The biosynthesis of prostaglandins and leukotrienes proceeds through the formation of chemically reactive intermediates leukotriene A 4 (LTA 4 ) and prostaglandin H 2 (PGH 2 ) which in aqueous solutions have chemical half-lives of 3 s and 3 min, respectively. Prostacyclin (PGI 2 ) is another chemically reactive prostanoid that has a chemical half-life of 3-4 min. The recent development of reversed phase HPLC stationary phases that are stable to elevated pH (pH 10 -12) without significant column damage has permitted direct analysis of these acid-sensitive eicosanoids. Using electrospray ionization, molecular anions [M Ϫ H] Ϫ of these compounds were observed at m/z 317 for LTA 4 and m/z 351 for both PGH 2 and PGI 2 . The mechanism of formation of ions derived from collisional activation of LTA 4 was studied using stable isotope labeled and chemical analogs of LTA 4 and found to involve formation of highly conjugated anions at m/z 261 and 163. The collisional activation of the molecular anion of PGH 2 yielded a product ion spectrum identical to that observed for the isomeric prostaglandins PGE 2 and PGD 2 . However, it was possible to baseline separate PGE 2 , PDG 2 , and PGH 2 by reversed phase HPLC using basic HPLC mobile phases. The collisional activation of PGI 2 led to a family of abundant ions including highly conjugated carbon-centered and oxygen-centered radical species (m/z 245 and 205) likely derived from the attack of the carboxylate anion on the cyclic enolether of PGI 2 as well as the most abundant product ion (m/z 215) which formed following loss of neutral hexanal and water. The structures of these product ions were consistent with high resolution measurements measured in a quadrupole time-of-flight mass

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“…The differential effect on medium PGE 2 levels during the isohydric reduction of medium pH between metabolic and respiratory acidosis could be due to differences in osteoblastic prostaglandin production or degradation. Changes in prostaglandin levels are generally thought to be due to differences in production; however, a previous study has shown that degradation is altered as a function of pH (71). PGE 2 dehydrates in aqueous solution to PGA 2 , and there is increased stability of PGE 2 in a model of metabolic acidosis compared with metabolic alkalosis (71).…”

Section: Discussionmentioning

confidence: 99%

“…Changes in prostaglandin levels are generally thought to be due to differences in production; however, a previous study has shown that degradation is altered as a function of pH (71). PGE 2 dehydrates in aqueous solution to PGA 2 , and there is increased stability of PGE 2 in a model of metabolic acidosis compared with metabolic alkalosis (71). However, the difference in stability between pH 6 and 8 is only ϳ1.2%, far less than the difference between metabolic acidosis and neutral medium observed in this study, suggesting that differences in degradation were not the cause of the metabolic acidosis-induced increase in PGE 2 levels.…”

Section: Discussionmentioning

confidence: 99%

Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release

Bushinsky

Parker

Alexander

et al. 2001

American Journal of Physiology-Renal Physiology

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. Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release. Am J Physiol Renal Physiol 281: F1058-F1066, 2001. First published July 12, 2001; 10.1152/ajprenal.00355.2001A decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO 3 Ϫ ]; metabolic acidosis) or to an increase in PCO2 (respiratory acidosis). In mammals, metabolic, but not respiratory, acidosis increases urine calcium excretion without altering intestinal calcium absorption, indicating that the additional urinary calcium is derived from bone. In cultured bone, chronic metabolic, but not respiratory, acidosis increases net calcium efflux (JCa), decreases osteoblastic collagen synthesis, and increases osteoclastic bone resorption. Metabolic acidosis increases bone PGE2 production, which is correlated with JCa, and inhibition of PGE2 production inhibits this acid-induced JCa. Given the marked differences in the osseous response to metabolic and respiratory acidosis, we hypothesized that incubation of neonatal mouse calvariae in medium simulating respiratory acidosis would not increase medium PGE 2 levels, as observed during metabolic acidosis. To test this hypothesis, we determined medium PGE2 levels and JCa from calvariae incubated at pH ϳ7.1 to model either metabolic (Met; [HCO 3 Ϫ ] ϳ11 mM) or respiratory (Resp; PCO2 ϳ83 Torr) acidosis, or at pH ϳ7.5 as a control (Ntl). We found that after 24-48 and 48-51 h in culture, periods when cell-mediated JCa predominates, medium PGE2 levels and JCa were increased with Met, but not Resp, compared with Ntl, and there was a direct correlation between medium PGE 2 levels and JCa. Thus metabolic, but not respiratory, acidosis induces the release of bone PGE2, which mediates JCa from bone. calvariae; osteoblasts; protons; pH IN HUMANS AND EXPERIMENTAL ANIMALS, chronic metabolic acidosis, a decrease in systemic pH induced by a decrease in serum bicarbonate concentration ([HCO 3 Ϫ ]), increases urine calcium excretion (15, 49, 51) without increasing intestinal calcium absorption (50, 51), resulting in a negative calcium balance (15,50,51). Because Ͼ98% of total body calcium is contained within the bone mineral (83), this negative calcium balance strongly implies a loss of bone calcium. Indeed, in humans dietary intake of acid precursors causes an apparent decrease in bone mineral content, which is reversed by the provision of alkali (50, 67).In contrast, chronic respiratory acidosis, a decrease in systemic pH induced by an increase in PCO 2 , appears to have little (30) or no (48, 65, 66) effect on urine calcium excretion. Clearly, any effect on urine calcium excretion is far less than that induced by metabolic acidosis (30). Serum calcium may increase slightly during respiratory acidosis (48). The lack of an appreciable change in urine calcium excretion during respiratory, compared with metabolic, acidosis suggests a marked difference in the osseous response to these two types of acidosis (10).We have extensively compared the response of cultured bone...

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[56] Physical chemistry, stability, and handling of prostaglandins E2, F2α, D2, and I2: A critical summary

Cited by 58 publications

References 27 publications

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

Mass spectrometric analysis of leukotriene A₄ and other chemically reactive metabolites of arachidonic acid

Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release

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[56] Physical chemistry, stability, and handling of prostaglandins E2, F2α, D2, and I2: A critical summary

Cited by 58 publications

References 27 publications

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

B1-Phytoprostanes Trigger Plant Defense and Detoxification Responses

Mass spectrometric analysis of leukotriene A4 and other chemically reactive metabolites of arachidonic acid

Metabolic, but not respiratory, acidosis increases bone PGE2levels and calcium release

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Mass spectrometric analysis of leukotriene A₄ and other chemically reactive metabolites of arachidonic acid

Metabolic, but not respiratory, acidosis increases bone PGE₂levels and calcium release