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Article: Extracellular Vesicles and Cancer Therapy: Insights into the Role of Oxidative Stress.

Ho, Jenni / Chaiswing, Luksana / St Clair, Daret K

2022 Volume 11, Issue 6

Abstract: Oxidative stress plays a significant role in cancer development and cancer therapy, and is a major contributor to normal tissue injury. The unique characteristics of extracellular vesicles (EVs) have made them potentially useful as a diagnostic tool in ... ...

Abstract	Oxidative stress plays a significant role in cancer development and cancer therapy, and is a major contributor to normal tissue injury. The unique characteristics of extracellular vesicles (EVs) have made them potentially useful as a diagnostic tool in that their molecular content indicates their cell of origin and their lipid membrane protects the content from enzymatic degradation. In addition to their possible use as a diagnostic tool, their role in how normal and diseased cells communicate is of high research interest. The most exciting area is the association of EVs, oxidative stress, and pathogenesis of numerous diseases. However, the relationship between oxidative stress and oxidative modifications of EVs is still unclear, which limits full understanding of the clinical potential of EVs. Here, we discuss how EVs, oxidative stress, and cancer therapy relate to one another; how oxidative stress can contribute to the generation of EVs; and how EVs' contents reveal the presence of oxidative stress. We also point out the potential promise and limitations of using oxidatively modified EVs as biomarkers of cancer and tissue injury with a focus on pediatric oncology patients.
Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11061194
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Article: Extracellular Vesicles and Cancer Therapy: Insights into the Role of Oxidative Stress

Ho, Jenni / Chaiswing, Luksana / St. Clair, Daret K.

Antioxidants. 2022 June 17, v. 11, no. 6

2022

Abstract	Oxidative stress plays a significant role in cancer development and cancer therapy, and is a major contributor to normal tissue injury. The unique characteristics of extracellular vesicles (EVs) have made them potentially useful as a diagnostic tool in that their molecular content indicates their cell of origin and their lipid membrane protects the content from enzymatic degradation. In addition to their possible use as a diagnostic tool, their role in how normal and diseased cells communicate is of high research interest. The most exciting area is the association of EVs, oxidative stress, and pathogenesis of numerous diseases. However, the relationship between oxidative stress and oxidative modifications of EVs is still unclear, which limits full understanding of the clinical potential of EVs. Here, we discuss how EVs, oxidative stress, and cancer therapy relate to one another; how oxidative stress can contribute to the generation of EVs; and how EVs’ contents reveal the presence of oxidative stress. We also point out the potential promise and limitations of using oxidatively modified EVs as biomarkers of cancer and tissue injury with a focus on pediatric oncology patients.
Keywords	biomarkers ; cancer therapy ; carcinogenesis ; diagnostic techniques ; lipids ; oxidative stress
Language	English
Dates of publication	2022-0617
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11061194
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Article: Chemotherapy-induced cognitive impairment: focus on the intersection of oxidative stress and TNFα

Rummel, Nicole G. / Chaiswing, Luksana / Bondada, Subbarao / St. Clair, Daret K. / Butterfield, D. Allan

Cellular and molecular life sciences. 2021 Oct., v. 78, no. 19-20

2021

Abstract: Chemotherapy-induced cognitive impairment (CICI) has been observed in a large fraction of cancer survivors. Although many of the chemotherapeutic drugs do not cross the blood–brain barrier, following treatment, the structure and function of the brain are ...

Abstract	Chemotherapy-induced cognitive impairment (CICI) has been observed in a large fraction of cancer survivors. Although many of the chemotherapeutic drugs do not cross the blood–brain barrier, following treatment, the structure and function of the brain are altered and cognitive dysfunction occurs in a significant number of cancer survivors. The means by which CICI occurs is becoming better understood, but there still remain unsolved questions of the mechanisms involved. The hypotheses to explain CICI are numerous. More than 50% of FDA-approved cancer chemotherapy agents are associated with reactive oxygen species (ROS) that lead to oxidative stress and activate a myriad of pathways as well as inhibit pathways necessary for proper brain function. Oxidative stress triggers the activation of different proteins, one in particular is tumor necrosis factor alpha (TNFα). Following treatment with various chemotherapy agents, this pro-inflammatory cytokine binds to its receptors at the blood–brain barrier and translocates to the parenchyma via receptor-mediated endocytosis. Once in brain, TNFα initiates pathways that may eventually lead to neuronal death and ultimately cognitive impairment. TNFα activation of the c-jun N-terminal kinases (JNK) and Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathways may contribute to both memory decline and loss of higher executive functions reported in patients after chemotherapy treatment. Chemotherapy also affects the brain’s antioxidant capacity, allowing for accumulation of ROS. This review expands on these topics to provide insights into the possible mechanisms by which the intersection of oxidative stress and TNFΑ are involved in chemotherapy-induced cognitive impairment.
Keywords	antioxidant activity ; blood-brain barrier ; brain ; cognitive disorders ; death ; drug therapy ; endocytosis ; memory disorders ; mitogen-activated protein kinase ; neurons ; oxidative stress ; reactive oxygen species ; transactivators ; tumor necrosis factor-alpha
Language	English
Dates of publication	2021-10
Size	p. 6533-6540.
Publishing place	Springer International Publishing
Document type	Article
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03925-4
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Article ; Online: Chemotherapy-induced cognitive impairment: focus on the intersection of oxidative stress and TNFα.

Rummel, Nicole G / Chaiswing, Luksana / Bondada, Subbarao / St Clair, Daret K / Butterfield, D Allan

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 19-20, Page(s) 6533–6540

Abstract: Chemotherapy-induced cognitive impairment (CICI) has been observed in a large fraction of cancer survivors. Although many of the chemotherapeutic drugs do not cross the blood-brain barrier, following treatment, the structure and function of the brain are ...

Abstract	Chemotherapy-induced cognitive impairment (CICI) has been observed in a large fraction of cancer survivors. Although many of the chemotherapeutic drugs do not cross the blood-brain barrier, following treatment, the structure and function of the brain are altered and cognitive dysfunction occurs in a significant number of cancer survivors. The means by which CICI occurs is becoming better understood, but there still remain unsolved questions of the mechanisms involved. The hypotheses to explain CICI are numerous. More than 50% of FDA-approved cancer chemotherapy agents are associated with reactive oxygen species (ROS) that lead to oxidative stress and activate a myriad of pathways as well as inhibit pathways necessary for proper brain function. Oxidative stress triggers the activation of different proteins, one in particular is tumor necrosis factor alpha (TNFα). Following treatment with various chemotherapy agents, this pro-inflammatory cytokine binds to its receptors at the blood-brain barrier and translocates to the parenchyma via receptor-mediated endocytosis. Once in brain, TNFα initiates pathways that may eventually lead to neuronal death and ultimately cognitive impairment. TNFα activation of the c-jun N-terminal kinases (JNK) and Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathways may contribute to both memory decline and loss of higher executive functions reported in patients after chemotherapy treatment. Chemotherapy also affects the brain's antioxidant capacity, allowing for accumulation of ROS. This review expands on these topics to provide insights into the possible mechanisms by which the intersection of oxidative stress and TNFΑ are involved in chemotherapy-induced cognitive impairment.
MeSH term(s)	Animals ; Antineoplastic Agents/adverse effects ; Brain/drug effects ; Brain/metabolism ; Chemotherapy-Related Cognitive Impairment/metabolism ; Humans ; Oxidative Stress/physiology ; Signal Transduction/drug effects ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Antineoplastic Agents ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2021-08-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03925-4
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Article ; Online: Mitochondrial superoxide targets energy metabolism to modulate epigenetic regulation of NRF2-mediated transcription.

Dhar, Sanjit K / Scott, Timothy / Wang, Chi / Fan, Teresa W M / St Clair, Daret K

Free radical biology & medicine

2021 Volume 179, Page(s) 181–189

Abstract: Mitochondria are central to the metabolic circuitry that generates superoxide radicals/anions ( ... ...

Abstract	Mitochondria are central to the metabolic circuitry that generates superoxide radicals/anions (O
MeSH term(s)	Acetylation ; Energy Metabolism/genetics ; Epigenesis, Genetic ; Histones/genetics ; Histones/metabolism ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Superoxides/metabolism
Chemical Substances	Histones ; NF-E2-Related Factor 2 ; Superoxides (11062-77-4)
Language	English
Publishing date	2021-12-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2021.12.309
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Article ; Online: A Redox-active Mn Porphyrin, MnTnBuOE-2-PyP

Chaiswing, Luksana / Yarana, Chontida / St Clair, William / Tovmasyan, Artak / Batinic-Haberle, Ines / Spasojevic, Ivan / St Clair, Daret

Oxidative medicine and cellular longevity

2022 Volume 2022, Page(s) 9664636

Abstract: We have employed a redox-active MnP (MnTnBuOE-2- ... ...

Abstract	We have employed a redox-active MnP (MnTnBuOE-2-PyP
MeSH term(s)	Antioxidants ; Carboplatin/pharmacology ; Carboplatin/therapeutic use ; Cell Line ; Female ; Humans ; Hydrogen Peroxide ; Metalloporphyrins/therapeutic use ; Ovarian Neoplasms/drug therapy ; Oxidation-Reduction ; Porphyrins ; Superoxide Dismutase
Chemical Substances	Antioxidants ; Metalloporphyrins ; Mn(III) meso-tetrakis(N-n-butoxyethylpyridinium-2-yl)porphyrin ; Porphyrins ; Hydrogen Peroxide (BBX060AN9V) ; Carboplatin (BG3F62OND5) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2022-05-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2022/9664636
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Article ; Online: UVB-induced inactivation of manganese-containing superoxide dismutase promotes mitophagy via ROS-mediated mTORC2 pathway activation.

Dhar, Sanjit K / Batinic-Haberle, Ines / St Clair, Daret K

The Journal of biological chemistry

2019 Volume 294, Issue 17, Page(s) 6831–6842

Abstract: Mitochondria are major sites of energy metabolism that influence numerous cellular events, including immunity and cancer development. Previously, we reported that the mitochondrion-specific antioxidant enzyme, manganese-containing superoxide dismutase ( ... ...

Abstract	Mitochondria are major sites of energy metabolism that influence numerous cellular events, including immunity and cancer development. Previously, we reported that the mitochondrion-specific antioxidant enzyme, manganese-containing superoxide dismutase (MnSOD), has dual roles in early- and late-carcinogenesis stages. However, how defective MnSOD impacts the chain of events that lead to cell transformation in pathologically normal epidermal cells that have been exposed to carcinogens is unknown. Here, we show that UVB radiation causes nitration and inactivation of MnSOD leading to mitochondrial injury and mitophagy. In keratinocytes, exposure to UVB radiation decreased mitochondrial oxidative phosphorylation, increased glycolysis and the expression of autophagy-related genes, and enhanced AKT Ser/Thr kinase (AKT) phosphorylation and cell growth. Interestingly, UVB initiated a prosurvival mitophagy response by mitochondria-mediated reactive oxygen species (ROS) signaling via the mammalian target of the mTOR complex 2 (mTORC2) pathway. Knockdown of rictor but not raptor abrogated UVB-induced mitophagy responses. Furthermore, fractionation and proximity-ligation assays reveal that ROS-mediated mTOC2 activation in mitochondria is necessary for UVB-induced mitophagy. Importantly, pretreatment with the MnSOD mimic MnTnBuOE-2-PyP
MeSH term(s)	Animals ; Autophagy/physiology ; Cell Line ; Mechanistic Target of Rapamycin Complex 2/metabolism ; Mice ; Mitochondria/drug effects ; Mitochondria/enzymology ; Mitochondria/metabolism ; Mitophagy/radiation effects ; Nitrates/metabolism ; Oxidation-Reduction ; Rapamycin-Insensitive Companion of mTOR Protein/physiology ; Reactive Oxygen Species/metabolism ; Regulatory-Associated Protein of mTOR/physiology ; Superoxide Dismutase/antagonists & inhibitors ; Ultraviolet Rays
Chemical Substances	Nitrates ; Rapamycin-Insensitive Companion of mTOR Protein ; Reactive Oxygen Species ; Regulatory-Associated Protein of mTOR ; Rptor protein, mouse ; rictor protein, mouse ; Superoxide Dismutase (EC 1.15.1.1) ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1)
Language	English
Publishing date	2019-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.RA118.006595
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Article: Chemotherapy-Induced Tissue Injury: An Insight into the Role of Extracellular Vesicles-Mediated Oxidative Stress Responses.

Yarana, Chontida / St Clair, Daret K

Antioxidants (Basel, Switzerland)

2017 Volume 6, Issue 4

Abstract: The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating ...

Abstract	The short- and long-term side effects of chemotherapy limit the maximum therapeutic dose and impair quality of life of survivors. Injury to normal tissues, especially chemotherapy-induced cardiomyopathy, is an unintended outcome that presents devastating health impacts. Approximately half of the drugs approved by the Food and Drug Administration for cancer treatment are associated with the generation of reactive oxygen species, and Doxorubicin (Dox) is one of them. Dox undergoes redox cycling by involving its quinone structure in the production of superoxide free radicals, which are thought to be instrumental to the role it plays in cardiomyopathy. Dox-induced protein oxidation changes protein function, translocation, and aggregation that are toxic to cells. To maintain cellular homeostasis, oxidized proteins can be degraded intracellularly by ubiquitin-proteasome pathway or by autophagy, depending on the redox status of the cell. Alternatively, the cell can remove oxidized proteins by releasing extracellular vesicles (EVs), which can be transferred to neighboring or distant cells, thereby instigating an intercellular oxidative stress response. In this article, we discuss the role of EVs in oxidative stress response, the potential of EVs as sensitive biomarkers of oxidative stress, and the role of superoxide dismutase in attenuating EV-associated oxidative stress response resulting from chemotherapy.
Language	English
Publishing date	2017-09-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox6040075
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Article ; Online: Hematopoietic Stem Cells: Normal Versus Malignant.

Carroll, Dustin / St Clair, Daret K

Antioxidants & redox signaling

2017 Volume 29, Issue 16, Page(s) 1612–1632

Abstract: Significance: The long-term hematopoietic stem cell (LT-HSC) demonstrates characteristics of self-renewal and the ability to manage expansion of the hematopoietic compartment while maintaining the capacity for differentiation into hematopoietic stem/ ... ...

Abstract	Significance: The long-term hematopoietic stem cell (LT-HSC) demonstrates characteristics of self-renewal and the ability to manage expansion of the hematopoietic compartment while maintaining the capacity for differentiation into hematopoietic stem/progenitor cell (HSPC) and terminal subpopulations. Deregulation of the HSPC redox environment results in loss of signaling that normally controls HSPC fate, leading to a loss of HSPC function and exhaustion. The characteristics of HSPC exhaustion via redox stress closely mirror phenotypic traits of hematopoietic malignancies and the leukemic stem cell (LSC). These facets elucidate the HSC/LSC redox environment as a druggable target and a growing area of cancer research. Recent Advances: Although myelosuppression and exhaustion of the hematopoietic niche are detrimental side effects of classical chemotherapies, new agents that modify the HSPC/LSC redox environment have demonstrated the potential for protection of normal HSPC function while inducing cytotoxicity within malignant populations. Critical issues: New therapies must preserve, or only slightly disturb normal HSPC redox balance and function, while simultaneously altering the malignant cellular redox state. The cascade nature of redox damage makes this a critical and delicate line for the development of a redox-based therapeutic index. Future directions: Recent evidence demonstrates the potential for redox-based therapies to impact metabolic and epigenetic factors that could contribute to initial LSC transformation. This is balanced by the development of therapies that protect HSPC function. This pushes toward therapies that may alter the HSC/LSC redox state but lead to initiation cell fate signaling lost in malignant transformation while protecting normal HSPC function. Antioxid. Redox Signal.
MeSH term(s)	Animals ; Hematopoietic Stem Cells/cytology ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Humans ; Oxidation-Reduction
Language	English
Publishing date	2017-12-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2017.7326
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Article ; Online: Dysregulation of cytokine mediated chemotherapy induced cognitive impairment.

Ren, Xiaojia / St Clair, Daret K / Butterfield, D Allan

Pharmacological research

2017 Volume 117, Page(s) 267–273

Abstract: One of the major complaints patients who survive cancer often make is chemotherapy induced cognitive impairment (CICI), which survivors often call "chemo brain." CICI is a side effect of chemotherapy due to the cytotoxicity and neurotoxicity of anti- ... ...

Abstract	One of the major complaints patients who survive cancer often make is chemotherapy induced cognitive impairment (CICI), which survivors often call "chemo brain." CICI is a side effect of chemotherapy due to the cytotoxicity and neurotoxicity of anti-cancer drugs causing structural and functional changes in brain, even when drugs that do not cross the blood brain barrier (BBB) are used. Diminished cognitive functions including diminution of learning and memory, concentration and attention, processing speed and executive functions that reduce quality of life and ability to work are common signs and symptoms of CICI. There still is not a clarified and complete mechanism for CICI, but researchers have pointed to several biochemical candidates. Chemotherapy-induced, cytokine-mediated involvement in CICI will be mainly discussed in this review paper with emphasis on different types of cytokines, correlated with BBB and epigenetic changes. Mechanisms of ROS-generating, anti-cancer drugs and their relation to cytokine-mediated CICI will be emphasized.
MeSH term(s)	Animals ; Antineoplastic Agents/adverse effects ; Blood-Brain Barrier/metabolism ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/metabolism ; Cytokines/metabolism ; Drug-Related Side Effects and Adverse Reactions/metabolism ; Humans ; Neoplasms/drug therapy
Chemical Substances	Antineoplastic Agents ; Cytokines
Language	English
Publishing date	2017-01-04
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2017.01.001
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