16,16-Dimethyl Prostaglandin E 2 Increases Survival in Mice Following Irradiation

Walden, Thomas L.; Patchen, Myra L.; Snyder, Stephen L.

doi:10.2307/3577044

Cited by 76 publications

(25 citation statements)

References 11 publications

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“…7,8 Recently, CAPE was investigated intensively in a number of animal models and various organs, including kidney, intestine, testis, spinal cord, hindlimb and lung. [7][8]19,20 It has been suggested that CAPE has protective effects against oxidative damage, which has been linked to its free radicalscavenging ability and anti-oxidant capacity. [20][21][22][23][24] Also, CAPE suppresses lipid peroxidation and inhibits lipoxygenase activity.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

Yildiz¹,

Soyuer²,

Saraymen³

et al. 2008

CIM

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Clin Invest Med 2008; 31 (5): E242-E247. AbstractPurpose: The prevention of radiation-induced pulmonary toxicity may help to improve radiation therapy in the cancer patient. The aim of this study was to investigate the pulmonary protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on radiation-induced lung injury in rats. Methods:30 Wistar albino rats were divided into three groups and treated with saline, Radiation (RT) and RT + CAPE respectively. All rats were treated with CAPE (50 μmol/kg i.p.) or saline. The first dose of CAPE was injected 24 h before radiation and application continued daily, with radiation in second day and 2 days more after the radiation treatment. Radiation dose was 800 cGy for total body. At 72 hr after the last radiation application, under general anesthesia using ip ketamine, the lungs were removed immediately after decapitation. After sacrification, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) activities and malondiadehyde (MDA) levels were evaluated in lung tissue. Results: The level of malondialdehyde (MDA) was higher in the RT group (233.4±1.5 nmol/g protein) than in both the control (131.8±0.92) and the RT + CAPE (151.4±1.8) groups (P < 0.001). However, CAT activity was decreased in the RT group (7.26±0.27 Umg protein) compared with control (8.49±0.51) and increased again in the RT + CAPE group (8.31±0.56; P<0.001). In accord with CAT activity, SOD activity in the RT group (0.42±0.07 nmolMDA/g wet tissue) was different from the control (0.78±0.02) and RT + CAPE (0.86±0.06) groups (P< 0.001). Conclusion: CAPE aplication with radiation therapy attenuated radiation induced pulmonary injury in vivo, possibly by its antioxidant effect.When radiation is absorbed by a biological material, free oxygen radicals are produced. The radicals are highly reactive molecules and, via chemical bonds that produce chemical changes, initiate a chain of events that result in biological damage. They can be produced either directly in the target molecule (usually DNA) or indirectly in other cellular molecules and they diffuse far enough to reach and damage critical targets. Most indirect effects occur by free radicals produced in water, since water makes up 70-80 % of mammalian cells. 1 In this way, chemotherapy and radiotherapy eliminate cancer cells, but their nonspecific targeting also destroys normal, healthy cells, particularly in epithelial tissues. Damage to the epithelium of the respiratory tract results in a pathologic condition known as pneumonitis . 2 Radiation (RT) is frequently used to treat tumors in and around the thorax. In these patients, RT-induced lung injury is common, occurring in 5% to 20% of patients with lung cancer. The incidence is somewhat less, 5% to 15%, for patients with tumors such as mediastinal lymphoma and breast cancer . 3 ORIGINAL RESEARCH

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Section: Discussionmentioning

confidence: 99%

Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

Yildiz¹,

Soyuer²,

Saraymen³

et al. 2008

CIM

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“…In addition, previous results indicated that spermatogonial stem cells also become less sensitive towards the induction of reciprocal translocations by higher doses of X-irradiation (Sankaranarayanan et al, 1995). So far only prostaglandin-mediated protection responses of in i o cell renewal systems as a whole, such as bone marrow (Hanson & Ainsworth, 1985 ;Walden et al, 1987), hair follicles (Geng et al, 1992), intestine (Hanson & Thomas, 1983) or germinal epithelium, have been described. In the present study we have further dissected this response and show for the first time that the protective effect is clearly present in the stem cell compartment -and, moreover, for both proliferating and quiescent stem cells.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it was demonstrated that various prostaglandins, or synthetic analogues such as misoprostol, protected the mucosa of the digestive tract from injury by non-steroidal anti-inflammatory agents, heat, acids and bases (Robert et al, 1979) or X-irradiation (Hanson & Thomas, 1983). Also other cell renewal systems such as bone marrow (Hanson & Ainsworth, 1985 ;Walden et al, 1987) and hair follicles (Geng et al, 1992) have been found to become more radioresistant by prostaglandin treatment. The mechanism for the radioprotective effect is unknown.…”

Section: Introductionmentioning

confidence: 99%

Radioprotective effect of misoprostol on mouse spermatogonial stem cells

Rooij

Beek

Rutgers³

et al. 1998

Genet. Res.

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The radioprotective effects of misoprostol, a synthetic stable analogue of prostaglandin E1, on spermatogonial stem cells of C3H/HeH x 101/F1 hybrid mice (3H1) were analysed by establishing dose--response relationships for stem cell killing by X-rays in mice that were pretreated with misoprostol. Spermatogonial stem cell killing was studied through determination of the percentage of tubular cross-sections showing repopulation at 10 days after irradiation. In control mice, the D0 values ranged between 1.7 and 3.6 Gy, dependent on the stage of the cycle of the seminiferous epithelium the cells were in. As found previously, proliferating spermatogonial stem cells were much more radioresistant than quiescent stem cells. In the misoprostol-pretreated animals the spermatogonial stem cells were more radioresistant, the D0 values ranging from 3.6 to 5.0 Gy. Both proliferating and quiescent spermatogonial stem cells were protected by misoprostol. As the dose--response curves in control and misoprostol-pretreated mice showed about the same extrapolation number to the y-axis it was concluded that the misoprostol pretreatment did not alter the kinetics of the repopulation process.

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“…Initially it was proposed that the augmentation of radioresponse induced by indomethacin could be due to lowering PGs in tumour tissues. The effects of PGs on radioprotection are, however, not clear: some authors reported that PGs might act as radioprotectors (Hanson & Ainsworth, 1985;Walden et al, 1987), whereas others (Milas et al, 1990) proposed an opposite effect.…”

Section: Radiothinlayer Chromatographymentioning

confidence: 99%

“…Apart from the fact that the mechanisms by which indomethacin potentiates tumour radioresponse are still unclear to date, it appears that an increased tumour response might be achieved by lowering PGs in the tumour. This, however, would imply that PGs are not radioprotective agents as has been suggested by Hanson & Ainsworth (1985) or Walden et al (1987). Milas and coworkers (1990) have also found that potentiation of the tumour radioresponse induced by indomethacin is more significant when it is given after rather than before irradiation.…”

mentioning

confidence: 95%

Acetylsalicylic acid (ASA) protects the prostaglandin-cAMP-system of human hypernephroma cells against irradiation-induced alterations

E²,

Pirker³

et al. 1993

Br J Cancer

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Summary There is abundant evidence that inhibitors of prostaglandin (PG) 3.6nM; PGI2: Bmax = 325 ± 194 fmol mg-protein, Kd = 6.8 ± 7.1nM) were significantly (P < 0.01) diminished.However, irradiation had no significant effect on PG bindig sites in ASA-pretreated cells (PGEI:Bmax =699 ± 240fmolmg-protein, Kd = 3.5 + 1.8nM; iloprost: Bmax = 766 ± 452 fmol mg-' protein, Kd = 3.2 ± 2.2nM). Although there was no significant difference in the basal values for cAMP between control and ASA-treated group cells, the PG-induced cAMP-production was less pronounced in the control group.Taken together, the findings suggest that ASA may modify the radioresponse of cultured human hypernephroma cells by preventing the decrease of PG binding sites induced by irradiation.

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16,16-Dimethyl Prostaglandin E 2 Increases Survival in Mice Following Irradiation

Cited by 76 publications

References 11 publications

Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

Radioprotective effect of misoprostol on mouse spermatogonial stem cells

Acetylsalicylic acid (ASA) protects the prostaglandin-cAMP-system of human hypernephroma cells against irradiation-induced alterations

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