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Abedi-Valugerdi, Manuchehr
Publications (10 of 19) Show all publications
Calado Botelho, S., Saghafian, M., Pavlova, S., Hassan, M., DePierre, J. W. & Abedi-Valugerdi, M. (2015). Complement activation is involved in the hepatic injury caused by high-dose exposure of mice to perfluorooctanoic acid. Chemosphere, 129(SI), 225-231
Open this publication in new window or tab >>Complement activation is involved in the hepatic injury caused by high-dose exposure of mice to perfluorooctanoic acid
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2015 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 129, no SI, p. 225-231Article in journal (Refereed) Published
Abstract [en]

High-dose exposure of mice to perfluorooctanoate (PFOA) induces both hepatotoxicity and immunotoxicity. Here, we characterized the effects of TO-day dietary treatment with PFOA (0.002-0.02%, w/w) on the liver and complement system of male C57BL/6 mice. At all four doses, this compound caused hepatomegaly and reduced the serum level of triglycerides (an indicator for activation of the peroxisome proliferator-activated receptor-alpha (PPAR alpha)). At the highest dose (0.02%, w/w), this hepatomegaly was associated with the hepatic injury, as reflected in increased activity of alanine aminotranferase (ALAT) in the serum, severe hepatocyte hypertrophy and hepatocellular necrosis. PFOA-induced hepatic injury was associated with in vivo activation of the complement system as indicated by (i) significant attenuation of the serum activities of both the classical and alternative pathways; (ii) a marked reduction in the serum level of the complement factor 0; and (iii) deposition of the complement factor C3 fragment (C3a) in the hepatic parenchyma. PFOA did not activate the alternative pathway of complement in vitro. At doses lower than 0.02%, PFOA induced hepatocyte hypertrophy without causing liver injury or activating complement. These results reveal substantial involvement of activation of complement in the pathogenesis of PFOA-induced hepatotoxicity.

Keywords
Complement system, Complement factor C3, Hepatotoxicity, Liver injury, Perfluorooctanoate, Peroxisome proliferator-activated receptor alpha
National Category
Biological Sciences
Identifiers
urn:nbn:se:su:diva-117762 (URN)10.1016/j.chemosphere.2014.06.093 (DOI)000353732600029 ()
Available from: 2015-06-09 Created: 2015-06-01 Last updated: 2022-02-23Bibliographically approved
Bogdanska, J., Sundström, M., Bergström, U., Borg, D., Abedi-Valugerdi, M., Bergman, Å., . . . Nobel, S. (2014). Tissue distribution of S-35-labelled perfluorobutanesulfonic acid in adult mice following dietary exposure for 1-5 days. Chemosphere, 98, 28-36
Open this publication in new window or tab >>Tissue distribution of S-35-labelled perfluorobutanesulfonic acid in adult mice following dietary exposure for 1-5 days
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2014 (English)In: Chemosphere, ISSN 0045-6535, E-ISSN 1879-1298, Vol. 98, p. 28-36Article in journal (Refereed) Published
Abstract [en]

Perfluorobutanesulfonyl fluoride (PBSF) has been introduced as a replacement for its eight-carbon homolog perfluorooctanesulfonyl fluoride (POSF) in the manufacturing of fluorochemicals. Fluorochemicals derived from PBSF may give rise to perfluorobutanesulfonic acid (PFBS) as a terminal degradation product. Although basic mammalian toxicokinetic data exist for PFBS, information on its tissue distribution has only been reported in one study focused on rat liver. Therefore, here we characterized the tissue distribution of PFBS in mice in the same manner as we earlier examined its eight-carbon homolog perfluorooctanesulfonate (PFOS) to allow direct comparisons. Following dietary exposure of adult male C57/BL6 mice for 1,3 or 5 d to 16 mg S-35-PFBS kg(-1) d(-1), both scintillation counting and whole-body autoradiography (WBA) revealed the presence of PFBS in all of the 20 different tissues examined, demonstrating its ability to leave the bloodstream and enter tissues. After 5 d of treatment the highest levels were detected in liver, gastrointestinal tract, blood, kidney, cartilage, whole bone, lungs and thyroid gland. WBA revealed relatively high levels of PFBS in male genital organs as well, with the exception of the testis. The tissue levels increased from 1 to 3 d of exposure but appeared thereafter to level-off in most cases. The estimated major body compartments were whole bone, liver, blood, skin and muscle. This exposure to PFBS resulted in 5-40-fold lower tissue levels than did similar exposure to PFOS, as well as in a different pattern of tissue distribution, including lower levels in liver and lungs relative to blood.

Keywords
Perfluorobutanesulfonic acid, Perfluorooctanesulfonic acid, Tissue distribution, Liquid scintillation, Autoradiography, Mice
National Category
Biological Sciences Chemical Sciences
Identifiers
urn:nbn:se:su:diva-102278 (URN)10.1016/j.chemosphere.2013.09.062 (DOI)000331679600003 ()
Note

AuthorCount:8;

Available from: 2014-04-04 Created: 2014-03-31 Last updated: 2022-02-28Bibliographically approved
Qazi, M. R., Hassan, M., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2013). Both sub-acute, moderate-dose and short-term, low-dose dietary exposure of mice to perfluorooctane sulfonate exacerbates concanavalin A-induced hepatitis. Toxicology Letters, 217(1), 67-74
Open this publication in new window or tab >>Both sub-acute, moderate-dose and short-term, low-dose dietary exposure of mice to perfluorooctane sulfonate exacerbates concanavalin A-induced hepatitis
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2013 (English)In: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 217, no 1, p. 67-74Article in journal (Refereed) Published
Abstract [en]

Exposure of rodents to perfluorooctane sulfonate (PFOS) induces pronounced hepatomegaly associated with significant alterations in hepatic histophysiology and immune status. The present investigation was designed to evaluate the effects of this perfluorochemical on immune-mediated liver damage. Accordingly, the influence of both sub-acute (10 days), moderate-dose (0.004%, w/w = 6 +/- 1.3 mg/kg body weight/day) or short-term (28 days), low-dose (0.0001%, w/w = 144 +/- 4 mu g/kg body weight/day) dietary pretreatment with PFOS on the development of concanavalin A (Con A)-induced liver damage in mice was examined. With either regimen of exposure, PFOS exacerbated the acute liver damage caused by Con A, i.e., elevated serum levels of transaminases and led to more pronounced damage of hepatic tissue. This exacerbation was associated with either reduced (moderate dose) or unaltered (low dose) hepatic levels of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). Moreover, hepatic DNA fragmentation was enhanced, particularly following short-term exposure to a low-dose. Our findings suggest that exposure to PFOS may sensitize hepatic parenchymal cells to other insults that activate the hepatic immune system and thereby exacerbate liver damage during acute inflammation.

Keywords
Concanavalin A, Pro-inflammatory cytokines, Hepatitis, Hepatomegaly, Perfluorooctane sulfonate
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:su:diva-88276 (URN)10.1016/j.toxlet.2012.12.001 (DOI)000313708000008 ()
Note

AuthorCount:5;

Available from: 2013-03-13 Created: 2013-03-12 Last updated: 2022-02-24Bibliographically approved
Sadeghi, B., Al-Chaqmaqchi, H., Al-Hashmi, S., Brodin, D., Hassan, Z., Abedi-Valugerdi, M., . . . Hassan, M. (2013). Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target?. Bone Marrow Transplantation, 48(2), 284-293
Open this publication in new window or tab >>Early-phase GVHD gene expression profile in target versus non-target tissues: kidney, a possible target?
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2013 (English)In: Bone Marrow Transplantation, ISSN 0268-3369, E-ISSN 1476-5365, Vol. 48, no 2, p. 284-293Article in journal (Refereed) Published
Abstract [en]

GVHD is a major complication after allo-SCT. In GVHD, some tissues like liver, intestine and skin are infiltrated by donor T cells while others like muscle are not. The mechanism underlying targeted tropism of donor T cells is not fully understood. In the present study, we aim to explore differences in gene expression profile among target versus non-target tissues in a mouse model of GVHD based on chemotherapy conditioning. Expression levels of JAK-signal transducers and activators of transcription (STAT), CXCL1, ICAM1 and STAT3 were increased in the liver and remained unchanged (or decreased) in the muscle and kidney after conditioning. At the start of GVHD the expression levels of CXCL9, ITGb2, SAA3, MARCO, TLR and VCAM1 were significantly higher in the liver or kidney compared with the muscle of GVHD animals. Moreover, biological processes of inflammatory reactions, leukocyte migration, response to bacterium and chemotaxis followed the same pattern. Our data show that both chemotherapy and allogenicity exclusively induce expression of inflammatory genes in target tissues. Moreover, gene expression profile and histopathological findings in the kidney are similar to those observed in the liver of GVHD mice. Bone Marrow Transplantation (2013) 48, 284-293; doi:10.1038/bmt.2012.120; published online 23 July 2012

Keywords
gene expression, GVHD, kidney, target tissues, mouse model
National Category
Biophysics Cancer and Oncology Hematology Immunology
Identifiers
urn:nbn:se:su:diva-88683 (URN)10.1038/bmt.2012.120 (DOI)000315239200026 ()
Funder
Swedish Cancer Society
Note

AuthorCount:8;

Available from: 2013-03-26 Created: 2013-03-25 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Hassan, M., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2013). Sub-acute, moderate-dose, but not short-term, low-dose dietary pre-exposure of mice to perfluorooctanoate aggravates concanavalin A-induced hepatitis. Toxicology Letters, 219(1), 1-7
Open this publication in new window or tab >>Sub-acute, moderate-dose, but not short-term, low-dose dietary pre-exposure of mice to perfluorooctanoate aggravates concanavalin A-induced hepatitis
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2013 (English)In: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 219, no 1, p. 1-7Article in journal (Refereed) Published
Abstract [en]

Exposure of mice to perfluorooctanoate (PFOA) evokes pronounced hepatomegaly along with significant alterations in both the histological structure and immune status of the liver. The present study was designed to evaluate the effects of this perfluorochemical on immune-mediated liver damage. In this connection, the influence of both sub-acute (10 days), moderate-dose (0.002% w/w = 3 +/- 0.7 mg/kg body weight/day) and short-term (28 days), low-dose (0.00005% w/w = 70 +/- 2 mu g/kg body weight/day) dietary pretreatment with PFOA on the development of concanavalin A (Con A)-induced liver damage in mice was examined. With sub-acute, moderate, but not short-term, low-dose exposure, PFOA aggravated the acute liver damage caused by Con A, i.e., elevated serum levels of transaminases and led to more pronounced damage of hepatic tissue. This aggravation was associated with significantly enhanced hepatic level of interleukin-6 (IL-6), but unaltered hepatic levels of tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) and interleukin-4 (IL-4). Moreover, hepatic DNA fragmentation was not changed by subacute exposure to the moderate-dose. Our findings imply that exposure to PFOA may sensitize hepatic parenchymal cells to other toxicants that activate the hepatic immune system and thereby aggravate liver injury during acute inflammation. 

Keywords
Concanavalin A, Interleukin 6, Hepatitis, Hepatomegaly, Perfluorooctanoate
National Category
Biological Sciences Pharmacology and Toxicology
Identifiers
urn:nbn:se:su:diva-89853 (URN)10.1016/j.toxlet.2013.02.017 (DOI)000317348100001 ()
Note

AuthorCount:5;

Available from: 2013-05-14 Created: 2013-05-14 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2012). High-dose dietary exposure of mice to perfluorooctanoate or perfluorooctane sulfonate exerts toxic effects on myeloid and B-lymphoid cells in the bone marrow and these effects are partially dependent on reduced food Consumption. Food and Chemical Toxicology, 50(9), 2955-2963
Open this publication in new window or tab >>High-dose dietary exposure of mice to perfluorooctanoate or perfluorooctane sulfonate exerts toxic effects on myeloid and B-lymphoid cells in the bone marrow and these effects are partially dependent on reduced food Consumption
2012 (English)In: Food and Chemical Toxicology, ISSN 0278-6915, E-ISSN 1873-6351, Vol. 50, no 9, p. 2955-2963Article in journal (Refereed) Published
Abstract [en]

It is well established that exposure of mice to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) exerts adverse effects on the thymus and spleen. Here, we characterize the effects of a 10-day dietary treatment with these compounds (0.001-0.02%, w/w) on the bone marrow (BM) of mice. At a dose of 0.02%, both compounds reduced food consumption and caused atrophy of the thymus and spleen. At this same dose, histopathological and flow cytometric analysis revealed that (i) the total numbers of BM as well as the numbers of myeloid, pro/pre B, immature B and early mature B cells were all reduced significantly; and (ii) these adverse effects were reversed either partially or completely 10 days after withdrawal of these compounds. At the lower dose of 0.002%, only PFOA reduced the B-lymphoid cell population. Finally, mice fed an amount of diet equivalent to that consumed by the animals exposed to 0.02% PFOA also exhibited atrophy of the thymus and spleen, and a reduction in the number of B-lymphoid population, without affecting myeloid cells. Thus, in mice, immunotoxic doses of PFOA or PFOS induce adverse effects on the myeloid and B-lymphoid cells in the BM, in part as a consequence of reduced food consumption.

Keywords
Perfluorooctane sulfonate, Perfluorooctanoate, Bone marrow, Myeloid cells, B-lymphoid cells, Food restriction
National Category
Food Science
Identifiers
urn:nbn:se:su:diva-81257 (URN)10.1016/j.fct.2012.06.023 (DOI)000308624500001 ()
Note

AuthorCount:4;

Available from: 2012-10-15 Created: 2012-10-15 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Abedi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2011). Characterization of the Hepatic and Splenic Immune Status and Immunoglobulin Synthesis in Aged Male Mice Lacking the Peroxisome Proliferator-Activated Receptor-Alpha (PPAR alpha). Scandinavian Journal of Immunology, 73(3), 198-207
Open this publication in new window or tab >>Characterization of the Hepatic and Splenic Immune Status and Immunoglobulin Synthesis in Aged Male Mice Lacking the Peroxisome Proliferator-Activated Receptor-Alpha (PPAR alpha)
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2011 (English)In: Scandinavian Journal of Immunology, ISSN 0300-9475, E-ISSN 1365-3083, Vol. 73, no 3, p. 198-207Article in journal (Refereed) Published
Abstract [en]

It is now well established that the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR alpha) is expressed in different types of immune cells and plays a pivotal role in the regulation of age-related production of inflammatory cytokines. However, the role(s) of this receptor in the regulation of immune cell homoeostasis in ageing non-lymphoid and lymphoid organs has not yet been resolved. We examine this issue here by evaluating the hepatic and splenic immune status and immunoglobulin (Ig) production in male PPAR alpha-null mice and their wild-type littermates at one and 2 years of age. In comparison with the age-matched control animals, PPAR alpha-null mice exhibited age-related elevations in the numbers of total, as well as of phenotypically distinct subpopulations of intrahepatic immune cells (IHIC) and splenocytes. Moreover, at 2 years of age, these alterations in hepatic immune cells were accompanied by significant increases in hepatic levels of the pro-inflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interferon-gamma (IFN-gamma), in combination with the development of hepatic inflammatory loci containing mixtures of leucocytes. Alterations in splenocytes of old PPAR alpha-null mice were also accompanied by increases in cellularity of both white and red pulps of the spleen. Furthermore, these same animals exhibited pronounced increases in the numbers of splenic plasma cells and enhanced production of Ig of different isotypes, including IgG1, IgG2a and IgE. Thus, our findings indicate that upon ageing, PPAR alpha plays a crucial role in regulating the total numbers, compositions and functions of immune cells in both lymphoid and non-lymphoid immune organs of mice.

National Category
Immunology
Identifiers
urn:nbn:se:su:diva-67925 (URN)10.1111/j.1365-3083.2010.02495.x (DOI)000287092100003 ()
Note
authorCount :5Available from: 2012-01-02 Created: 2012-01-02 Last updated: 2022-02-24Bibliographically approved
Bogdanska, J., Borg, D., Sundström, M., Bergström, U., Halldin, K., Abedi-Valugerdi, M., . . . Nobel, S. (2011). Tissue distribution of (35)S-labelled perfluorooctane sulfonate in adult mice after oral exposure to a low environmentally relevant dose or a high experimental dose. Toxicology, 284(1-3), 54-62
Open this publication in new window or tab >>Tissue distribution of (35)S-labelled perfluorooctane sulfonate in adult mice after oral exposure to a low environmentally relevant dose or a high experimental dose
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2011 (English)In: Toxicology, ISSN 0300-483X, E-ISSN 1879-3185, Vol. 284, no 1-3, p. 54-62Article in journal (Refereed) Published
Abstract [en]

The widespread environmental pollutant perfluorooctane sulfonate (PFOS), detected in most animal species including the general human population, exerts several effects on experimental animals, e.g., hepatotoxicity, immunotoxicity and developmental toxicity. However, detailed information on the tissue distribution of PFOS in mammals is scarce and, in particular, the lack of available information regarding environmentally relevant exposure levels limits our understanding of how mammals (including humans) may be affected. Accordingly, we characterized the tissue distribution of this compound in mice, an important experimental animal for studying PFOS toxicity. Following dietary exposure of adult male C57/BL6 mice for 1-5 days to an environmentally relevant (0.031 mg/kg/day) or a 750-fold higher experimentally relevant dose (23 mg/kg/day) of (35)S-PFOS, most of the radioactivity administered was recovered in liver, bone (bone marrow), blood, skin and muscle, with the highest levels detected in liver, lung, blood, kidney and bone (bone marrow). Following high daily dose exposure, PFOS exhibited a different distribution profile than with low daily dose exposure, which indicated a shift in distribution from the blood to the tissues with increasing dose. Both scintillation counting (with correction for the blood present in the tissues) and whole-body autoradiography revealed the presence of PFOS in all 19 tissues examined, with identification of thymus as a novel site for localization for PFOS and bone (bone marrow), skin and muscle as significant body compartments for PFOS. These findings demonstrate that PFOS leaves the bloodstream and enters most tissues in a dose-dependent manner.

Keywords
PFOS, Distribution, Hemoglobin, Scintillation, Autoradiography, Adult mice
National Category
Biological Sciences Chemical Sciences
Identifiers
urn:nbn:se:su:diva-67584 (URN)10.1016/j.tox.2011.03.014 (DOI)000291140300008 ()
Note
authorCount :10Available from: 2011-12-29 Created: 2011-12-29 Last updated: 2022-02-28Bibliographically approved
Qazi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2010). 28-Day dietary exposure of mice to a low total dose (7 mg/kg) of perfluorooctanesulfonate (PFOS) alters neither the cellular compositions of the thymus and spleen nor humoral immune responses: Does the route of administration play a pivotal role in PFOS-induced immunotoxicity?. Toxicology, 267(03-jan), 132-139
Open this publication in new window or tab >>28-Day dietary exposure of mice to a low total dose (7 mg/kg) of perfluorooctanesulfonate (PFOS) alters neither the cellular compositions of the thymus and spleen nor humoral immune responses: Does the route of administration play a pivotal role in PFOS-induced immunotoxicity?
2010 (English)In: Toxicology, ISSN 0300-483X, E-ISSN 1879-3185, Vol. 267, no 03-jan, p. 132-139Article in journal (Refereed) Published
Abstract [en]

Short-term exposure of mice to high doses of perfluorooctanesulfonate (PFOS), an ubiquitous and highly persistent environmental contaminant, induces various metabolic changes and toxic effects, including immunotoxicity. However, extrapolation of these findings to the long-term, low-dose exposures to which humans are subject is highly problematic. In this connection, recent studies have concluded that sub-chronic (28-day) exposure of mice by oral gavage to doses of PFOS that result in serum levels comparable to those found in general human populations suppress adaptive immunity. Because of the potential impact of these findings on environmental research and monitoring, we have examined here whether sub-chronic dietary exposure (a major route of human exposure) to a similarly low-dose of PFOS also suppress adaptive immune responses. Dietary treatment of male B6C3F1 mice for 28 days with a dose of PFOS that resulted in a serum concentration of 11 mu g/ml (ppm) significantly reduced body weight gain and increased liver mass. However, this treatment did not alter the cellular compositions of the thymus and spleen; the number of splenic cells secreting IgM antibodies against sheep red blood cell (SRBC); serum levels of IgM and IgG antibodies specifically towards SRBC; or circulating levels of IgM antibodies against the T-cell-independent antigen trinitrophenyl conjugated to lipopolysaccharide (TNP-LPS). These findings indicate that such sub-chronic dietary exposure of mice to PFOS resulting in serum levels approximately 8-85-fold greater than those observed in occupationally exposed individuals does not exert adverse effects on adaptive immunity.

Keywords
Humoral immune responses, T-cell-independent antigen, T-cell-dependent antigen, Perfluorooctanesulfonate (PFOS)
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:su:diva-50059 (URN)10.1016/j.tox.2009.10.035 (DOI)000274588700017 ()
Note

authorCount :4

Available from: 2011-01-03 Created: 2010-12-21 Last updated: 2022-02-24Bibliographically approved
Qazi, M. R., Abedi, M. R., Nelson, B. D., DePierre, J. W. & Abedi-Valugerdi, M. (2010). Dietary exposure to perfluorooctanoate or perfluorooctane sulfonate induces hypertrophy in centrilobular hepatocytes and alters the hepatic immune status in mice. International Immunopharmacology, 10(11), 1420-7
Open this publication in new window or tab >>Dietary exposure to perfluorooctanoate or perfluorooctane sulfonate induces hypertrophy in centrilobular hepatocytes and alters the hepatic immune status in mice
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2010 (English)In: International Immunopharmacology, ISSN 1567-5769, E-ISSN 1878-1705, Vol. 10, no 11, p. 1420-7Article in journal (Refereed) Published
Abstract [en]

It is well established that exposure of mice to perfluorooctanoate (PFOA) or perfluorooctane sulfonate (PFOS) induces hepatomegaly and, concurrently, immunotoxicity. However, the effects of these perfluorochemicals on the histology and immune status of the liver have not been yet investigated and we have examined these issues here. Dietary treatment of male C57BL/6 mice with 0.002% (w/w) PFOA or 0.005% (w/w) PFOS for 10 days resulted in significant reductions in serum levels of cholesterol and triglycerides, a moderate increase in the serum activity of alkaline phosphatase (ALP) and hepatomegaly, without affecting other immune organs. This hepatomegaly was associated with marked hypertrophy of the centrilobular hepatocytes, with elevated numbers of cytoplasmic acidophilic granules and occasional mitosis. Furthermore, dietary exposure to PFOA or PFOS altered the hepatic immune status: whereas exposure to PFOA enhanced the numbers of total, as well as of phenotypically distinct subpopulations of intrahepatic immune cells (IHIC), and in particular the presumptive erythrocyte progenitor cells, treatment with PFOS enhanced only the numbers of hepatic cells that appear immunophenotypically to be erythrocyte progenitors, without affecting other types of IHIC. In addition, exposure to these compounds attenuated hepatic levels of tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-4 (IL-4). Furthermore, the exposed animals exhibited a significant increase in hepatic levels of erythropoietin, a hormone required for erythropoiesis. Thus, in mice, PFOA- and PFOS-induced hepatomegaly is associated with significant alterations in hepatic histophysiology and immune status, as well as induction of hepatic erythropoiesis.

Keywords
Perfluorooctane sulfonate, Perfluorooctanoate, Hepatomegaly, Hepatic immune system, Intrahepatic immune cells, Erythropoiesis, Erythropoietin
National Category
Natural Sciences
Research subject
Biophysics; Biochemistry
Identifiers
urn:nbn:se:su:diva-51627 (URN)10.1016/j.intimp.2010.08.009 (DOI)20816993 (PubMedID)
Available from: 2011-01-11 Created: 2011-01-11 Last updated: 2022-02-24Bibliographically approved
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