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Article ; Online: Bisphenol A (BPA) exposure aggravates hepatic oxidative stress and inflammatory response under hypertensive milieu - Impact of low dose on hepatocytes and influence of MAPK and ER stress pathways.

Nagarajan, Manikandan / Maadurshni, Gobichettipalayam Balasubramaniam / Manivannan, Jeganathan

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2023 Volume 183, Page(s) 114197

Abstract: Human exposure to the hazardous chemical, Bisphenol A (BPA), is almost ubiquitous. Due to the prevalence of hypertension (CVD risk factor) in the aged human population, it is necessary to explore its adverse effect in hypertensive subjects. The current ... ...

Abstract	Human exposure to the hazardous chemical, Bisphenol A (BPA), is almost ubiquitous. Due to the prevalence of hypertension (CVD risk factor) in the aged human population, it is necessary to explore its adverse effect in hypertensive subjects. The current study exposed the Nω-nitro-l-arginine methyl ester (L-NAME) induced hypertensive Wistar rats to human exposure relevant low dose of BPA (50 μg/kg) for 30 days period. The liver biochemical parameters, histopathology, immunohistochemistry, gene expression (RT-qPCR), trace elements (ICP-MS), primary rat hepatocytes cell culture and metabolomic (1H NMR) assessments were performed. Results illustrate that BPA exposure potentiates/aggravates hypertension induced tissue abnormalities (hepatic fibrosis), oxidative stress, ACE activity, malfunction of the antioxidant system, lipid abnormalities and inflammatory factor (TNF-α and IL-6) expression. Also, in cells, BPA increased ROS generation, mitochondrial dysfunction and lipid peroxidation without any impact on cytotoxicity and caspase 3 and 9 activation. Notably, BPA exposure modulate lipid metabolism (cholesterol and fatty acid) in primary hepatocytes. Finally, the influence of ERK1/2, p38MAPK, ER stress and oxidative stress during relatively high dose of BPA elicited cytotoxicity was observed. Therefore, a precise hazardous risk investigation of BPA exposure in hypertensive populations is highly recommended.
MeSH term(s)	Humans ; Rats ; Animals ; Aged ; Rats, Wistar ; Liver ; Hepatocytes ; Oxidative Stress ; Benzhydryl Compounds/pharmacology ; Hypertension/chemically induced
Chemical Substances	bisphenol A (MLT3645I99) ; Benzhydryl Compounds
Language	English
Publishing date	2023-11-28
Publishing country	England
Document type	Journal Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2023.114197
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Article ; Online: Exposure to low dose of Bisphenol A (BPA) intensifies kidney oxidative stress, inflammatory factors expression and modulates Angiotensin II signaling under hypertensive milieu.

Nagarajan, Manigandan / Maadurshni, Gobichettipalayam Balasubramaniam / Manivannan, Jeganathan

Journal of biochemical and molecular toxicology

2023 Volume 38, Issue 1, Page(s) e23533

Abstract: Humans are constantly exposed to low concentrations of ubiquitous environmental pollutant, Bisphenol A (BPA). Due to the prevalence of hypertension (one of the major risk factors of cardiovascular disease [CVD]) in the population, it is necessary to ... ...

Abstract	Humans are constantly exposed to low concentrations of ubiquitous environmental pollutant, Bisphenol A (BPA). Due to the prevalence of hypertension (one of the major risk factors of cardiovascular disease [CVD]) in the population, it is necessary to explore the adverse effect of BPA under hypertension associated pathogenic milieu. The current study exposed the Nω-nitro-l-arginine methyl ester (L-NAME) induced hypertensive Wistar rats to low dose BPA (50 μg/kg) for 30 days period. In tissue samples immunohistochemistry, real-time quantitative polymerase chain reaction and enzymatic assays were conducted. Moreover, studies on primary kidney cell culture were employed to explore the impact of low dose of BPA exposure at nanomolar level (20-80 nM range) on renal cells through various fluorescence assays. The observed results illustrate that BPA exposure potentiates/aggravates hypertension induced tissue abnormalities (renal fibrosis), oxidative stress (ROS generation), elevated angiotensin-converting enzyme activity, malfunction of the antioxidant and tricarboxylic acid cycle enzymes, tissue lipid abnormalities and inflammatory factor expression (both messenger RNA and protein level of TNF-α and IL-6). Further, in vitro exposure of nM levels of BPA to primary kidney cells modulates oxidative stress (both superoxide and total ROS), mitochondrial physiology (reduced mitochondrial transmembrane potential-∆ψm) and lipid peroxidation in a dose dependent manner. In addition, angiotensin II induced ROS generation was aggravated further by BPA during coexposure in kidney cells. Therefore, during risk assessment, a precise investigation on BPA exposure in hypertensive (CVD vulnerable) populations is highly suggested.
MeSH term(s)	Rats ; Humans ; Animals ; Angiotensin II/pharmacology ; Reactive Oxygen Species/metabolism ; Rats, Wistar ; Oxidative Stress ; Kidney ; Hypertension/chemically induced ; Hypertension/metabolism ; Benzhydryl Compounds/toxicity ; Phenols
Chemical Substances	Angiotensin II (11128-99-7) ; bisphenol A (MLT3645I99) ; Reactive Oxygen Species ; Benzhydryl Compounds ; Phenols
Language	English
Publishing date	2023-09-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	1410020-4
ISSN	1099-0461 ; 1095-6670
ISSN (online)	1099-0461
ISSN	1095-6670
DOI	10.1002/jbt.23533
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Article: Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome - A multi-omics big data study.

Manivannan, Jeganathan / Sundaresan, Lakshmikirupa

Gene reports

2021 Volume 25, Page(s) 101312

Abstract: Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that led to more than 800,00 deaths and continues to be a major threat worldwide. The scientific community has been studying ... ...

Abstract	Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that led to more than 800,00 deaths and continues to be a major threat worldwide. The scientific community has been studying the risk factors associated with SARS-CoV-2 infection and pathogenesis. Recent studies highlight the possible contribution of atmospheric air pollution, specifically particulate matter (PM) exposure as a co-factor in COVID-19 severity. Hence, meaningful translation of suitable omics datasets of SARS-CoV-2 infection and PM exposure is warranted to understand the possible involvement of airborne exposome on COVID-19 outcome. Publicly available transcriptomic data (microarray and RNA-Seq) related to COVID-19 lung biopsy, SARS-CoV-2 infection in epithelial cells and PM exposure (lung tissue, epithelial and endothelial cells) were obtained in addition with proteome and interactome datasets. System-wide pathway/network analysis was done through appropriate software tools and data resources. The primary findings are; 1. There is no robust difference in the expression of SARS-CoV-2 entry factors upon particulate exposure, 2. The upstream pathways associated with upregulated genes during SARS-CoV-2 infection considerably overlap with that of PM exposure, 3. Similar pathways were differentially expressed during SARS-CoV-2 infection and PM exposure, 4. SARS-CoV-2 interacting host factors were predicted to be associated with the molecular impact of PM exposure and 5. Differentially expressed pathways during PM exposure may increase COVID-19 severity. Based on the observed molecular mechanisms (direct and indirect effects) the current study suggests that airborne PM exposure has to be considered as an additional co-factor in the outcome of COVID-19.
Language	English
Publishing date	2021-08-12
Publishing country	United States
Document type	Journal Article
ISSN	2452-0144
ISSN	2452-0144
DOI	10.1016/j.genrep.2021.101312
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Article ; Online: Exposure to a "safe" dose of environmental pollutant bisphenol A elevates oxidative stress and modulates vasoactive system in hypertensive rats.

Nagarajan, Manigandan / Raja, Boobalan / Manivannan, Jeganathan

Human & experimental toxicology

2021 Volume 40, Issue 12_suppl, Page(s) S654–S665

Abstract: Due to the prevalence of hypertension (one of the major risk factors of CVD) in the population, it is necessary to explore the adverse effects of daily tolerable and "safe" dose of bisphenol A (BPA) under hypertensive conditions. The current study ... ...

Abstract	Due to the prevalence of hypertension (one of the major risk factors of CVD) in the population, it is necessary to explore the adverse effects of daily tolerable and "safe" dose of bisphenol A (BPA) under hypertensive conditions. The current study exposed the Nω-nitro-l-arginine methyl ester (L-NAME, 40 mg/kg b.w/day) induced hypertensive Wistar rats to BPA (50 μg/kg b.w/day) by oral administration along with appropriate controls for 30 days period. The results illustrate that a 'safe' dose of BPA does not influence the systolic blood pressure (SBP) and levels of circulatory biomarkers of tissue damage. On the other hand, BPA exposure significantly (
MeSH term(s)	Animals ; Benzhydryl Compounds/toxicity ; Blood Pressure/drug effects ; Hypertension/metabolism ; Male ; Oxidative Stress/drug effects ; Phenols/toxicity ; Rats ; Rats, Wistar ; Thiobarbituric Acid Reactive Substances/metabolism
Chemical Substances	Benzhydryl Compounds ; Phenols ; Thiobarbituric Acid Reactive Substances ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2021-11-19
Publishing country	England
Document type	Journal Article
ZDB-ID	1027454-6
ISSN	1477-0903 ; 0144-5952 ; 0960-3271
ISSN (online)	1477-0903
ISSN	0144-5952 ; 0960-3271
DOI	10.1177/09603271211053285
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Article: Systems toxicology approach explores target-pathway relationship and adverse health impacts of ubiquitous environmental pollutant bisphenol A.

Nagarajan, Manigandan / Maadurshni, Gobichettipalayam Balasubramaniam / Manivannan, Jeganathan

Journal of toxicology and environmental health. Part A

2021 Volume 85, Issue 6, Page(s) 217–229

Abstract: The effects of environmental chemicals on health outcomes may be underestimated due to deficiency of knowledge regarding the actions of compounds on toxico-pathogenic mechanisms underlying biological systems outcomes. In this regard, the current study ... ...

Abstract	The effects of environmental chemicals on health outcomes may be underestimated due to deficiency of knowledge regarding the actions of compounds on toxico-pathogenic mechanisms underlying biological systems outcomes. In this regard, the current study aimed to explore the potential target-pathway-disease relationship attributed to bisphenol A (BPA) responses in target tissues. Computational methods including reverse pharmacophore mapping approach, structural similarity based search and kinome wide interaction profiling were employed with molecular docking validation. Gene ontology (GO) enrichment analysis and protein-protein interaction (PPI) network based illustrations were utilized to prioritize target-pathway and disease relationships. Data illustrated that BPA possessed multi-target nature since this chemical potentially interacted with various protein targets where many of these were validated through docking. Potential BPA targets were significantly enriched to various cellular signaling pathways including steroid biosynthesis, peroxisome proliferator-activated receptor gamma (PPARℽ) and cancer. Further, hypertension was prioritized as disease target. In addition, BPA targeted 17 cell signaling kinases encompassed in the human kinome. In addition, inflammatory (5-LO) and apoptosis regulators (Bcl-X and Bcl-2) were also explored as novel targets. Evidence indicates that the multi-target nature and plausible mechanisms underlying BPA actions in a system wide manner aids toward understanding of adverse effects. This observation may lead us to more precise method to elucidate the toxico-pathogenic mechanisms of BPA with an environmental health perspective.
MeSH term(s)	Benzhydryl Compounds/chemistry ; Benzhydryl Compounds/toxicity ; Endocrine Disruptors/toxicity ; Environmental Pollutants/toxicity ; Gene Ontology ; Humans ; Molecular Docking Simulation ; Phenols/chemistry ; Phenols/toxicity ; Proteome ; Signal Transduction
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Environmental Pollutants ; Phenols ; Proteome ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2021-10-27
Publishing country	England
Document type	Journal Article
ZDB-ID	1413345-3
ISSN	1528-7394 ; 0098-4108 ; 1087-2620
ISSN	1528-7394 ; 0098-4108 ; 1087-2620
DOI	10.1080/15287394.2021.1994492
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Zs.A 1268: Show issues

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Article ; Online: Al

Maadurshni, Gobichettipalayam Balasubramaniam / Tharani, Ganeshmurthy Kanniamal / Udayakumar, Inbamani / Nagarajan, Manigandan / Manivannan, Jeganathan

Environmental science and pollution research international

2022 Volume 29, Issue 36, Page(s) 54250–54263

Abstract: Recent evidences illustrated that the release of aluminum oxide nanoparticles ( ... ...

Abstract	Recent evidences illustrated that the release of aluminum oxide nanoparticles (Al
MeSH term(s)	Aluminum Oxide/toxicity ; Animals ; Apoptosis ; Chick Embryo ; JNK Mitogen-Activated Protein Kinases/metabolism ; Nanoparticles/toxicity ; Tumor Necrosis Factor-alpha/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Tumor Necrosis Factor-alpha ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Aluminum Oxide (LMI26O6933)
Language	English
Publishing date	2022-03-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-19243-6
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Article ; Online: System-wide health risk prediction for 4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene(MBP), a major active metabolite of environmental pollutant and food contaminant - Bisphenol A.

Maadurshni, Gobichettipalayam Balasubramaniam / Nagarajan, Manigandan / Priyadharshini, Saravanan / Singaravelu, Usha / Manivannan, Jeganathan

Toxicology

2022 Volume 485, Page(s) 153414

Abstract: Human exposure to plastic contaminated foods and environmental micro/nano plastic derived chemicals necessitates system-wide health risk assessment. Hence, current study intend to explore the mode of action (MoA) based adverse outcome pathways of 4- ... ...

Abstract	Human exposure to plastic contaminated foods and environmental micro/nano plastic derived chemicals necessitates system-wide health risk assessment. Hence, current study intend to explore the mode of action (MoA) based adverse outcome pathways of 4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP), the major active metabolite of bisphenol A (BPA). The computational study employed broad range of target prediction, systems biology tools and molecular docking protocols. Further, validation of MBP targets was done using protein-ligand fluorescence quenching assay, endothelial cell culture and chicken embryo vascular angiogenesis models. Interestingly, the current results illustrate that various physiological signaling pathways (MAPK and VEGF related angiogenesis signaling) and disease progression pathways (hypertension, cancer and endocrine disorders) were enriched as potential targets of MBP. Further, docking studies highlights the possible binding mechanism of MBP with important targets including endothelial nitric oxide synthase (eNOS) and serum albumin (BSA). In addition, the validation studies on MBP-BSA interaction (fluorescence quenching), eNOS derived nitric oxide (NOx) generation in endothelial cells and chicken embryo angiogenesis support the system-wide impacts of MBP with highlights on cardiovascular pathogenesis. Thus, the current observation provides novel insights into the system wide impacts of MBP for the futuristic health risk assessment of plastic derived chemicals.
MeSH term(s)	Animals ; Humans ; Chick Embryo ; Molecular Docking Simulation ; Environmental Pollutants ; Endothelial Cells/metabolism ; Benzhydryl Compounds/chemistry
Chemical Substances	4-methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene ; bisphenol A (MLT3645I99) ; Environmental Pollutants ; Benzhydryl Compounds
Language	English
Publishing date	2022-12-29
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	184557-3
ISSN	1879-3185 ; 0300-483X
ISSN (online)	1879-3185
ISSN	0300-483X
DOI	10.1016/j.tox.2022.153414
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Zs.A 888: Show issues

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Article ; Online: Exposure to zinc oxide nanoparticles (ZnO-NPs) induces cardiovascular toxicity and exacerbates pathogenesis - Role of oxidative stress and MAPK signaling.

Nagarajan, Manigandan / Maadurshni, Gobichettipalayam Balasubramaniam / Tharani, Ganeshmurthy Kanniamal / Udhayakumar, Inbamani / Kumar, Gayathri / Mani, Krishna Priya / Sivasubramanian, Jeganathan / Manivannan, Jeganathan

Chemico-biological interactions

2021 Volume 351, Page(s) 109719

Abstract: The precise toxico-pathogenic effects of zinc oxide nanoparticles (ZnO-NPs) on the cardiovascular system under normal and cardiovascular disease (CVD) risk factor milieu are unclear. In this study, we have investigated the dose-dependent effects of ZnO- ... ...

Abstract	The precise toxico-pathogenic effects of zinc oxide nanoparticles (ZnO-NPs) on the cardiovascular system under normal and cardiovascular disease (CVD) risk factor milieu are unclear. In this study, we have investigated the dose-dependent effects of ZnO-NPs on developing chicken embryo and cell culture (H9c2 cardiomyoblast, HUVEC and aortic VSMC) models. In addition, the potentiation effect of ZnO-NPs on simulated risk factor conditions was evaluated using; 1. Reactive oxygen species (ROS) induced cardiac remodeling, 2. Angiotensin-II induced cardiac hypertrophy, 3. TNF-α induced HUVEC cell death and 4. Inorganic phosphate (Pi) induced aortic VSMC calcification models. The observed results illustrates that ZnO-NPs exposure down regulates vascular development and elevates oxidative stress in heart tissue. At the cellular level, ZnO-NPs exposure reduced the cell viability and increased the intracellular ROS generation, lipid peroxidation and caspase-3 activity in a dose-dependent manner in all three cell types. In addition, ZnO-NPs exposure significantly suppressed the endothelial nitric oxide (NO) generation, cardiac Ca
MeSH term(s)	Animals ; Apoptosis/drug effects ; Cardiomegaly/chemically induced ; Cardiomegaly/metabolism ; Cardiotoxicity ; Cardiotoxins/toxicity ; Chickens ; Embryo, Nonmammalian/drug effects ; Heart/drug effects ; Human Umbilical Vein Endothelial Cells ; Humans ; MAP Kinase Signaling System/drug effects ; Metal Nanoparticles/toxicity ; Mitochondria/drug effects ; Oxidative Stress/drug effects ; Rats ; Zinc Oxide/toxicity
Chemical Substances	Cardiotoxins ; Zinc Oxide (SOI2LOH54Z)
Language	English
Publishing date	2021-10-23
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2021.109719
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Article: Al2O3 nanoparticles trigger the embryonic hepatotoxic response and potentiate TNF-α-induced apoptosis—modulatory effect of p38 MAPK and JNK inhibitors

Maadurshni, Gobichettipalayam Balasubramaniam / Tharani, Ganeshmurthy Kanniamal / Udayakumar, Inbamani / Nagarajan, Manigandan / Manivannan, Jeganathan

Environmental science and pollution research. 2022 Aug., v. 29, no. 36

2022

Abstract: Recent evidences illustrated that the release of aluminum oxide nanoparticles (Al₂O₃-NPs) into the biosphere may pose risk to the environment and cause adverse effects on living organisms including humans. The current study assessed the hepatotoxic ... ...

Abstract	Recent evidences illustrated that the release of aluminum oxide nanoparticles (Al₂O₃-NPs) into the biosphere may pose risk to the environment and cause adverse effects on living organisms including humans. The current study assessed the hepatotoxic effects of Al₂O₃-NPs on developing chicken embryo and cell culture models. Results demonstrated that Al₂O₃-NPs exposure causes histological abnormalities and increased the level of tissue damage markers (ALP, AST, and ALT) in the embryonic liver. Furthermore, increased oxidative stress (TBARS) and impaired function of antioxidant enzymes (SOD, CAT, and GPx) were also observed. Moreover, it adversely affects red blood cells (RBC) morphology, liver metabolism, and stress response gene expression (HO-1 and NQO-1). Dose-dependent ROS generation and cytotoxic response in addition to potentiating effect on tumor necrosis factor alpha (TNF-α)-induced apoptosis (caspase-3 activity) were also observed. Inhibition of p38 mitogen-activated protein kinase (p38 MAPK) and c-Jun N-terminal kinase (JNK) pathways modulates Al₂O₃-NPs-induced apoptosis in HepG2 cells. Novel mechanisms behind embryonic hepatotoxicity, cytotoxic potentiating effects, and possible prevention strategies have been explored.
Keywords	aluminum oxide ; apoptosis ; biosphere ; caspase-3 ; cell culture ; chick embryos ; cytotoxicity ; dose response ; gene expression ; hepatotoxicity ; histology ; liver ; metabolism ; mitogen-activated protein kinase ; oxidative stress ; pollution ; research ; risk ; stress response ; tumor necrosis factor-alpha
Language	English
Dates of publication	2022-08
Size	p. 54250-54263.
Publishing place	Springer Berlin Heidelberg
Document type	Article
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-19243-6
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: In-situ biofabrication of bacterial nanocellulose (BNC)/graphene oxide (GO) nano-biocomposite and study of its cationic dyes adsorption properties.

Walling, Bendangtula / Bharali, Pranjal / Ramachandran, D / Viswanathan, K / Hazarika, Swapnali / Dutta, Nipu / Mudoi, Pronab / Manivannan, Jeganathan / Manjunath Kamath, S / Kumari, Sony / Vishwakarma, Vinita / Sorhie, Viphrezolie / Gogoi, Bhagyudoy / Acharjee, Shiva Aley / Alemtoshi

International journal of biological macromolecules

2023 Volume 251, Page(s) 126309

Abstract: In the present study, bacterial nanocellulose/graphene oxide nano-biocomposites (BNC-GO-NBCs) were fabricated by Komagataeibacter saccharivorans NUWB1 using an in-situ method involving three time-dependent approaches. Physicochemical studies showed that ... ...

Abstract	In the present study, bacterial nanocellulose/graphene oxide nano-biocomposites (BNC-GO-NBCs) were fabricated by Komagataeibacter saccharivorans NUWB1 using an in-situ method involving three time-dependent approaches. Physicochemical studies showed that the chosen dried BNC-GO-NBC possessed a three-dimensional interconnected porous structure of BNC with GO layers embedded within the BNC fibrils. BNC-GO-NBC had a crystallinity index of 74.21 %, higher thermostability up to 380 °C and could withstand a tensile load of 84.72 MPa. N
Language	English
Publishing date	2023-08-12
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	282732-3
ISSN	1879-0003 ; 0141-8130
ISSN (online)	1879-0003
ISSN	0141-8130
DOI	10.1016/j.ijbiomac.2023.126309
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