5-aminolevulinic acid-induced alterations of oxidative metabolism in sedentary and exercise-trained rats

1992 ◽  
Vol 72 (1) ◽  
pp. 226-230 ◽  
Author(s):  
B. Pereira ◽  
R. Curi ◽  
E. Kokubun ◽  
E. J. Bechara
Keyword(s):  
Superoxide Dismutase ◽  
Citrate Synthase ◽  
Aminolevulinic Acid ◽  
Acute Intermittent Porphyria ◽  
Serum Lactate ◽  
Rat Liver Mitochondria ◽  
Control Group ◽  
Type I

5-Aminolevulinic acid (ALA), a heme precursor that accumulates in acute intermittent porphyria patients and lead-exposed individuals, has previously been shown to autoxidize with generation of reactive oxygen species and to cause in vitro oxidative damage to rat liver mitochondria. We now demonstrate that chronically ALA-treated rats (40 mg/kg body wt every 2 days for 15 days) exhibit decreased mitochondrial enzymatic activities (superoxide dismutase, citrate synthase) in liver and soleus (type I, red) and gastrocnemius (type IIb, white) muscle fibers. Previous adaptation of rats to endurance exercise, indicated by augmented (cytosolic) CuZn-superoxide dismutase (SOD) and (mitochondrial) Mn-SOD activities in several organs, does not protect the animals against liver and soleus mitochondrial damage promoted by intraperitoneal injections of ALA. This is suggested by loss of citrate synthase and Mn-SOD activities and elevation of serum lactate levels, concomitant to decreased glycogen content in soleus and the red portion of gastrocnemius (type IIa) fibers of both sedentary and swimming-trained ALA-treated rats. In parallel, the type IIb gastrocnemius fibers, which are known to obtain energy mainly by glycolysis, do not undergo these biochemical changes. Consistently, ALA-treated rats under swimming training reach fatigue significantly earlier than the control group. These results indicate that ALA may be an important prooxidant in vivo.

scholarly journals 5-Aminolevulinic Acid-Based Photodynamic Therapy Pretreatment Mitigates Ultraviolet A-Induced Oxidative Photodamage

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Hui Hua ◽  
Jiawei Cheng ◽  
Wenbo Bu ◽  
Juan Liu ◽  
Weiwei Ma ◽  
...  
Keyword(s):  
Aminolevulinic Acid ◽  
Epidermal Keratinocytes ◽  
Control Group ◽  
Hacat Cells ◽  
Ultraviolet A ◽  
Hairless Mice ◽  
Human Epidermal Keratinocytes ◽  
Experimental Group

Aim. To determine whether 5-aminolevulinic acid-based photodynamic therapy (ALA-PDT) is effective in combating ultraviolet A- (UVA-) induced oxidative photodamage of hairless mice skin in vivo and human epidermal keratinocytes in vitro. Methods. In in vitro experiments, the human keratinocyte cell line (HaCaT cells) was divided into two groups: the experimental group was treated with ALA-PDT and the control group was left untreated. Then, the experimental group and the control group of cells were exposed to 10 J/m2 of UVA radiation. ROS, O2− species, and MMP were determined by fluorescence microscopy; p53, OGG1, and XPC were determined by Western blot analysis; apoptosis was determined by flow cytometry; and 8-oxo-dG was determined by immunofluorescence. Moreover, HaCaT cells were also treated with ALA-PDT. Then, SOD1 and SOD2 were examined by Western blot analysis. In in vivo experiments, the dorsal skin of hairless mice was treated with ALA-PDT or saline-PDT, and then, they were exposed to 20 J/m2 UVA light. The compound 8-oxo-dG was detected by immunofluorescence. Conclusion. In human epidermal keratinocytes and hairless mice skin, UVA-induced oxidative damage can be prevented effectively with ALA-PDT pretreatment.

scholarly journals In Vivo Antiviral Effects of U18666A Against Type I Feline Infectious Peritonitis Virus

Pathogens ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 67 ◽  
Author(s):  
Tomoyoshi Doki ◽  
Tomoyo Tarusawa ◽  
Tsutomu Hohdatsu ◽  
Tomomi Takano
Keyword(s):  
Clinical Symptoms ◽  
Treated Group ◽  
Control Group ◽  
Type I ◽  
Feline Infectious Peritonitis Virus ◽  
Feline Infectious Peritonitis ◽  
Amphiphilic Drug ◽  
Antiviral Effects

Background: The cationic amphiphilic drug U18666A inhibits the proliferation of type I FIPV in vitro. In this study, we evaluated the in vivo antiviral effects of U18666A by administering it to SPF cats challenged with type I FIPV. Methods: Ten SPF cats were randomly assigned to two experimental groups. FIPV KU-2 were inoculated intraperitoneally to cats. The control group was administered PBS, and the U18666A-treated group was administered U18666A subcutaneously at 2.5 mg/kg on day 0, and 1.25 mg/kg on days 2 and 4 after viral inoculation. Results: Two of the five control cats administered PBS alone developed FIP. Four of the five cats administered U18666A developed no signs of FIP. One cat that temporarily developed fever, had no other clinical symptoms, and no gross lesion was noted on an autopsy after the end of the experiment. The FIPV gene was detected intermittently in feces and saliva regardless of the development of FIP or administration of U18666A. Conclusions: When U18666A was administered to cats experimentally infected with type I FIPV, the development of FIP might be suppressed compared with the control group. However, the number of animals with FIP is too low to establish anti-viral effect of U18666A in cats.

Experimental induced wound cicatrisation after highly diluted products treatment

2021 ◽  
Vol 11 (40) ◽  
pp. 211-212
Author(s):  
Fernando Fortunato Jeronimo ◽  
Jenifer Pendiuk Gonçalves ◽  
Katia Fialho Do Nascimento ◽  
Simone Martins De Oliveira ◽  
Carolina Camargo De Oliveira ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Inflammatory Cells ◽  
Control Group ◽  
Type I ◽  
Chelidonium Majus ◽  
Conium Maculatum ◽  
The Matrix ◽  
Aconitum Napellus

Introduction: Skin is an attractive target to study extracellular matrix, due to abundance in Connective tissue. In cases of injuries the first step is an inflammatory reaction and subsequent the healing that involves several changes in the matrix. These changes are fundamental to inflammatory cells activities allowing healing. Highly diluted products were shown to facilitate inflammatory mediators and to activate immune cells in vivo and in vitro, thus it can be effective to wound healing. Aims: This study aims to evaluate highly diluted products effects on inflammation and cicatrization process. Methodology: Three compounds (M8 (Aconitum napellus 20dH, Arsenicum album 18dH, Asa foetida 20dH, Calcarea carbonica 16dH, Conium maculatum 17dH, Ipecacuanha 13dH, Phosphorus 20dH, Rhus toxicodendron 17dH, Silicea 20dH, Sulphur 24dH, Thuja occidentalis 19dH), M1 (Chelidonium majus 20dH, Cinnamon 20dH, Echinaceae purpurea 20dH, Gelsemium sempervirens 20dH plus all M8 compounds) and Curcuma cH30 – simple product), were manipulated as a gel and applied on mice dorsal flank after incision and suture (approximately 1 cm and three points), for 3 consecutive days. After the treatments the scars were evaluated macroscopically, the animals were killed, the skin samples collected, fixed and processed for Hematoxilin-Eosin (HE) and Masson Tricromic (to observe the collagen fibers type I). The slices were analyzed and images collected by a light microscope Olympus BX51 with camera attached Olympus DP72. Results: It was observed a higher and faster rate of tissue epithelization in the treated groups after three days of gel-product application. This could be observed in lower rates in the control group (no treatment) - Figure 1 and 2). Regeneration and organization of connective tissue were proportional to epithelization the treated groups. We also observed evidences of changes in amount of neutrophils and fibroblasts, resulting in changes in the healing period. Analyses for these confirmations are in progress.

Chronic exercise enhances in vivo and in vitro cytotoxic mechanisms of natural immunity in mice

1993 ◽  
Vol 74 (1) ◽  
pp. 388-395 ◽  
Author(s):  
B. MacNeil ◽  
L. Hoffman-Goetz
Keyword(s):  
Citrate Synthase ◽  
Wheel Running ◽  
In Vitro Cytotoxicity ◽  
Treadmill Running ◽  
Pulmonary Vasculature ◽  
Control Group ◽  
Natural Immunity ◽  
Chronic Exercise

This study investigated the influence of 9 wk of chronic exercise on natural cytotoxicity in male C3H mice. Both in vivo cytotoxicity (pulmonary vasculature) and in vitro cytotoxicity (spleen) were determined for voluntary (wheel running; n = 30) and forced (treadmill running, 15 m/min, 30 min/day; n = 30) exercise protocols. A sedentary control group (n = 30) and a treadmill control group (5 m/min, 5 min/day; n = 30) were also included. After 9 wk of chronic exercise, submaximal exercise O2 uptake was reduced in the wheel-running group relative to that in sedentary or treadmill-trained mice. Maximal citrate synthase activity of soleus muscle was higher in treadmill-trained group compared with that in sedentary or wheel-running mice. Chronic exercise consistently reduced percent retention of CIRAS 3 tumor cells in the lungs of treadmill- (15.3 +/- 1.4) and wheel- (17.9 +/- 1.4) trained mice below that of sedentary (29.5 +/- 2.7) and treadmill control (25.8 +/- 1.8) groups (P < 0.001). Injection of anti-asialo GM1 (ASGM1) antibody increased tumor cell retention in the lungs for all groups but did not alter the differences between activity conditions. In vitro cytotoxicity was enhanced in treadmill- and wheel-trained mice relative to that in sedentary controls but was not elevated in the treadmill control group. Anti-ASGM1 injection eliminated in vitro cytotoxicity for all groups. Chronic exercise slightly increased the frequency of ASGM1-positive splenocytes in treadmill-trained mice only. These results indicate that chronic exercise enhances natural cytotoxic mechanisms in vivo and in vitro and that this enhancement is present for both forced and voluntary exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Arginine promotes porcine type I muscle fibres formation through improvement of mitochondrial biogenesis

2019 ◽  
Vol 123 (5) ◽  
pp. 499-507 ◽  
Author(s):  
Xiaoling Chen ◽  
Xiaoming Luo ◽  
Daiwen Chen ◽  
Bing Yu ◽  
Jun He ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
Basal Diet ◽  
Sirtuin 1 ◽  
Control Group ◽  
Muscle Fibres ◽  
Type I ◽  
Mrna Levels ◽  
Nuclear Respiratory Factor

AbstractThe present study aimed to investigate whether arginine (Arg) promotes porcine type I muscle fibres formation via improving mitochondrial biogenesis. In the in vivo study, a total of sixty Duroc × Landrace × Yorkshire weaning piglets with an average body weight of 6·55 (sd 0·36) kg were randomly divided into four treatments and fed with a basal diet or a basal diet supplemented with 0·5, 1·0 and 1·5 % l-Arg, respectively, in a 4-week trial. Results showed that dietary supplementation of 1·0 % Arg significantly enhanced the activity of succinate dehydrogenase, up-regulated the protein expression of myosin heavy chain I (MyHC I) and increased the mRNA levels of MyHC I, troponin I1, C1 and T1 (Tnni1, Tnnc1 and Tnnt1) in longissimus dorsi muscle compared with the control group. In addition, ATPase staining analysis indicated that 1·0 % Arg supplementation significantly increased the number of type I muscle fibres and significantly decreased the number of type II muscle fibres. Furthermore, 1·0 % Arg supplementation significantly up-regulated PPAR-γ coactivator-1α (PGC-1α), sirtuin 1 and cytochrome c (Cytc) protein expressions, increased PGC-1α, nuclear respiratory factor 1 (NRF1), mitochondria transcription factor B1 (TFB1M), Cytc and ATP synthase subunit C1 (ATP5G) mRNA levels and increased mitochondrial DNA content. In the in vitro study, mitochondrial complex I inhibitor rotenone (Rot) was used. We found that Rot annulled Arg-induced type I muscle fibres formation. Together, our results provide for the first time the evidence that Arg promotes porcine type I muscle fibres formation through improvement of mitochondrial biogenesis.

scholarly journals In vitro and in vivo tenocyte-protective effectiveness of dehydroepiandrosterone against high glucose-induced oxidative stress

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shintaro Mukohara ◽  
Yutaka Mifune ◽  
Atsuyuki Inui ◽  
Hanako Nishimoto ◽  
Takashi Kurosawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Achilles Tendon ◽  
Mrna Expression ◽  
High Glucose ◽  
Control Group ◽  
Type I

Abstract Background Dehydroepiandrosterone (DHEA), an adrenal steroid, has a protective role against diabetes. This study aimed to investigate the in vitro and in vivo protective effects of DHEA against high glucose-induced oxidative stress in tenocytes and tendons. Methods Tenocytes from normal Sprague-Dawley rats were cultured in low-glucose (LG) or high-glucose (HG) medium with or without DHEA. The experimental groups were: control group (LG without DHEA), LG with DHEA, HG without DHEA, and HG with DHEA. Reactive oxygen species (ROS) production, apoptosis, and messenger RNA (mRNA) expression of NADPH oxidase (NOX) 1 and 4, and interleukin-6 (IL-6) were determined. Further, diabetic rats were divided into a control group and a DHEA-injected group (DHEA group). NOX1 and NOX4 protein expression and mRNA expression of NOX1, NOX4, IL-6, matrix metalloproteinase (MMP)-2, tissue inhibitors of matrix metalloproteinase (TIMP)-2, and type I and III collagens in the Achilles tendon were determined. Results In rat tenocytes, DHEA decreased the expression of NOX1 and IL-6, ROS accumulation, and apoptotic cells. In the diabetic rat Achilles tendon, NOX1 protein expression and mRNA expression of NOX1, IL-6, MMP-2, TIMP-2, and type III collagen were significantly lower while type I collagen expression was significantly higher in the DHEA group than in the control group. Conclusions DHEA showed antioxidant and anti-inflammatory effects both in vitro and in vivo. Moreover, DHEA improved tendon matrix synthesis and turnover, which are affected by hyperglycemic conditions. DHEA is a potential preventive drug for diabetic tendinopathy.

scholarly journals In Vitro and in Vivo Tenocyte-protective Effectiveness of Dehydroepiandrosterone Against High Glucose-induced Oxidative Stress

2021 ◽  
Author(s):  
Shintaro Mukohara ◽  
Yutaka Mifune ◽  
Atsuyuki Inui ◽  
Hanako Nishimoto ◽  
Takashi Kurosawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Matrix Metalloproteinase ◽  
Protein Expression ◽  
Achilles Tendon ◽  
Mrna Expression ◽  
High Glucose ◽  
Control Group ◽  
Type I

Abstract BackgroundDehydroepiandrosterone (DHEA), an adrenal steroid, has a protective role against diabetes. The aim of this study was to investigate the in vitro and in vivo protective effects of DHEA against high glucose-induced oxidative stress in tenocytes and tendons. Methods In an in vitro study, tenocytes from normal Sprague-Dawley rats were cultured in low-glucose (LG) or high-glucose (HG) medium with or without DHEA. The experimental groups were: control group (LG without DHEA), LG with DHEA, HG without DHEA, and HG with DHEA. Reactive oxygen species (ROS) production, apoptosis, and messenger RNA (mRNA) expression of NADPH oxidase (NOX) 1 and 4, and interleukin-6 (IL-6) were determined. In the in vivo study, diabetic rats were divided into a control group and a DHEA-injected group (DHEA group). NOX1 and NOX4 protein expression and mRNA expression of NOX1, NOX4, IL-6, matrix metalloproteinase (MMP)-2, tissue inhibitors of matrix metalloproteinase (TIMP)-2, and type I and III collagens in the Achilles tendon were determined. Results In rat tenocytes, DHEA decreased the expression of NOX1 and IL-6, ROS accumulation, and apoptotic cells. In the diabetic rat Achilles tendon, NOX1 protein expression and mRNA expression of NOX1, IL-6, MMP-2, TIMP-2, and type III collagen were significantly lower, while type I collagen expression was significantly lower in the DHEA group.Conclusions DHEA showed antioxidant and anti-inflammatory effects both in vitro and in vivo. Moreover, DHEA improved tendon matrix synthesis and turnover which are affected by hyperglycemic conditions. DHEA could be a preventive drug for the diabetic tendinopathy.

Interferon Regulatory Factor 4 Is Not Required for Induction of Chronic Myeloid Leukaemia-Like Myeloproliferative Disease by Bcr/Abl in Mice.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2866-2866
Author(s):  
Anna Lena Illert ◽  
Cornelius Miething ◽  
Rebekka Grundler ◽  
Manuel Schmidt ◽  
Andreas Burchert ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
Plasma Cells ◽  
Pulmonary Haemorrhage ◽  
Myeloproliferative Disorder ◽  
Control Group ◽  
Type I ◽  
Myeloproliferative Disease

Abstract Interferon regulatory factors (IRF) are activating and/or repressing transcription factors induced by treatment with type I and II Interferon (IFN), other cytokines, receptor cross-linking and viral infection. In contrast to IRF-1 and IRF-2, which are widely expressed, IRF-4 and IRF-8 are tissue-restricted factors. IRF-8 is expressed mainly in cells of haematopoietic origin and has recently been shown to inhibit mitogenic activity of p210 Bcr/Abl-transformed myeloid progenitor cells by activating several genes that interfere with the c-Myc pathway. IRF-4 is most homologous with IRF-8 (approximately 70% overall homology) and its expression is highly restricted to lymphocytes of the B-cell type (pre-B, B, and plasma cells), mature T-cells and macrophages. Furthermore IRF-4 expression is significantly impaired in CML and AML patient samples predominately in T-cells. To examine a potential role of IRF-4 in Bcr/Abl mediated transformation we used a bone marrow transplant model (BMT). We transduced IRF-4 knockout (KO) bone marrow with retrovirus expressing p210 Bcr/Abl and transplanted it into lethally irradiated recipient C57/bl6 mice. For proper control we transplanted also wildtype (WT) bone marrow transduced with Bcr/Abl and mock transfected IRF-4 KO bone marrow (BM). All recipients transplanted with Bcr/Abl transduced BM (regardless of which IRF-4 KO or WT) developed rapidly a myeloproliferative disorder characterized by leukocytosis and expression of the myeloid lineage markers CD11b and Gr1. Surprisingly, IRF-4 KO Bcr/Abl infected BM recipient mice survived slightly longer than the control group transplanted with WT p210 BM (12 vs. 19 days). Histopathologic studies of the affected organs (spleen/lung) revealed extramedullary haematopoiesis in the spleens of both groups and a distinct infiltration of the tumor cells in the lung of WT Bcr/Abl transduced BM recipient mice, resulting in massive punctuated bleedings. Interestingly, preliminary analysis suggest a significantly reduced lung infiltration with almost no pulmonary bleedings in IRF-4 KO Bcr/Abl infected BM recipient mice, which we assume to be the reason for the differences in the overall survival. Taken together our data demonstrate that IRF-4 is not required for the induction of a myeloproliferative disorder by Bcr/Abl in vivo and for its ability to transform BM cells in vitro, but IRF-4 deficiency seems to have an impact on the fulminant pulmonary haemorrhage occurring in the murine CML-like disease.

scholarly journals Effects of low intensity laser in in vitro bacterial culture and in vivo infected wounds

2014 ◽  
Vol 41 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Pâmela Rosa Pereira ◽  
Josue Bruginski De Paula ◽  
Juliette Cielinski ◽  
Marcelo Pilonetto ◽  
Luiz Carlos Von Bahten
Keyword(s):  
Laser Therapy ◽  
Control Group ◽  
Type I ◽  
Low Intensity ◽  
Infected Wounds ◽  
Male Wistar Rats ◽  
Low Intensity Laser Therapy ◽  
Intensity Laser

OBJECTIVE: to compare the effects of low intensity laser therapy on in vitro bacterial growth and in vivo in infected wounds, and to analyze the effectiveness of the AsGa Laser technology in in vivo wound infections. METHODS: in vitro: Staphylococcus aureus were incubated on blood agar plates, half of them being irradiated with 904 nm wavelength laser and dose of 3J/cm2 daily for seven days. In vivo: 32 male Wistar rats were divided into control group (uninfected) and Experimental Group (Infected). Half of the animals had their wounds irradiated. RESULTS: in vitro: there was no statistically significant variation between the experimental groups as for the source plates and the derived ones (p>0.05). In vivo: there was a significant increase in the deposition of type I and III collagen in the wounds of the infected and irradiated animals when assessed on the fourth day of the experiment (p=0.034). CONCLUSION: low-intensity Laser Therapy applied with a wavelength of 904nm and dose 3J/cm2 did not alter the in vitro growth of S. aureus in experimental groups; in vivo, however, it showed significant increase in the deposition of type I and III collagen in the wound of infected and irradiated animals on the fourth day of the experiment.

Effects of Pentoxifylline on Peritoneal Fibroblasts and Silica-Induced Peritoneal Fibrosis

2003 ◽  
Vol 23 (3) ◽  
pp. 228-236 ◽  
Author(s):  
Cheng-Chung Fang ◽  
Ming-Nan Lai ◽  
Chiang-Ting Chien ◽  
Kuan-Yu Hung ◽  
Chien-Chen Tsai ◽  
...  
Keyword(s):  
Body Weight ◽  
Collagen Synthesis ◽  
Control Group ◽  
Type Iii Collagen ◽  
Type I ◽  
Dependent Manner ◽  
Peritoneal Fibrosis ◽  
Group 1

♦ Background Peritoneal fibrosis is a long-term complication following continuous ambulatory peritoneal dialysis (CAPD). Peritoneal fibroblasts may play an important role in peritoneal fibrosis. Up to now, the treatment of peritoneal fibrosis in patients with CAPD remains unsatisfactory. Pentoxifylline (PTX) is a xanthine derivative and is used in the treatment of peripheral vascular and cerebrovascular diseases. Several studies have demonstrated that PTX can ameliorate fibrosis of the skin, liver, and kidney. ♦ Objective To investigate the effect of PTX on in vitro growth and collagen synthesis of human peritoneal fibroblasts (HPFBs), and to evaluate the effects of PTX on silica-induced peritoneal fibrosis in vivo. ♦ Design and Measurements In the in vitro study, HPFBs were cultured from human omentum. The effect of PTX on the growth of serum-stimulated HPFBs was evaluated by MTT assay. The effect of PTX on the collagen synthesis of HPFB was measured by [3H]-proline incorporation. Expression of type I and type III collagen mRNA was evaluated by Northern blotting. The effects of PTX on matrix metalloproteinase (MMP) activity and cAMP level in HPFBs were measured by immunoassays. In the in vivo study, Wistar rats were randomly divided into five groups. All rats received intraperitoneal (IP) injection of silica suspension (250 mg/100 g body weight) on day 0. The rats of group 1 (control group) were injected with vehicle IP every day for 14 days. The rats of groups 2, 3, and 4 were injected with PTX (4 mg/100 g body weight) IP every day for 3, 7, and 14 days, respectively. The rats in group 5 received an intravenous infusion of PTX (8 mg/100 g body weight) every day for 7 days. On the 15th day after silica injection, all rats were sacrificed. Their parietal and visceral peritoneums were removed and processed for pathology, and the severity of fibrosis was measured and scored. ♦ Results: In vitro, PTX inhibited serum-stimulated HPFB growth (maximum was 93% at 1 mg PTX/mL) in a dose-dependent manner. Collagen synthesis by HPFB was reduced (47% at 1 mg PTX/mL), and collagen I and III mRNA expression in HPFBs was suppressed by PTX. The PTX did not affect the MMP (including MMP-1, MMP-8, and MMP-13) activities of HPFBs. The mechanism of PTX was through increasing cAMP by its phosphodiesterase inhibiting activity. In vivo, the severity of fibrosis was significantly reduced in groups 4 and 5 compared to group 1 ( p < 0.05). ♦ Conclusion These results suggest that PTX can inhibit growth of and collagen synthesis by HPFBs in vitro. The fibrosis derived from silica-induced peritonitis in vivo was also ameliorated by PTX. Therefore, pentoxifylline may have the potential to be used to treat peritoneal fibrosis in patients on CAPD.

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