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Article ; Online: Copper: From enigma to therapeutic target for neurological disorder.

Patwa, Jayant / Flora, Swaran Jeet Singh

Basic & clinical pharmacology & toxicology

2024 Volume 134, Issue 6, Page(s) 778–791

Abstract: Neurological disorders (NDs) have a negative impact on the lives of individuals. There could be two explanations for this: unclear aetiology and lack of effective therapy. However, research in the past few years has revealed the role of bio-metals ... ...

Abstract	Neurological disorders (NDs) have a negative impact on the lives of individuals. There could be two explanations for this: unclear aetiology and lack of effective therapy. However, research in the past few years has revealed the role of bio-metals dyshomeostasis in NDs. The imbalance in copper (Cu) concentration may be one of the main causative factors in NDs. In this review, we have discussed the role of Cu in NDs, especially Alzheimer's disease (AD), including the molecular mechanisms involved in Cu-associated NDs like oxidative stress, neuroinflammation, and protein misfolding. We have also summarized the recent Cu-targeting approaches and highlighted the in vitro and in vivo studies recently being reported on the subject. Based on the earlier published reports, it could be speculated that the Cu targeting strategy might be an interesting and potential therapeutic approach for NDs. Various difficulties must be overcome to develop safe and efficient Cu-targeting medications for NDs.
MeSH term(s)	Humans ; Copper/metabolism ; Animals ; Oxidative Stress/drug effects ; Nervous System Diseases/drug therapy ; Alzheimer Disease/drug therapy ; Alzheimer Disease/metabolism ; Neuroinflammatory Diseases/drug therapy
Language	English
Publishing date	2024-04-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.14010
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Article ; Online: Alpha Lipoic Acid and Monoisoamyl-DMSA Combined Treatment Ameliorates Copper-Induced Neurobehavioral Deficits, Oxidative Stress, and Inflammation.

Patwa, Jayant / Thakur, Ashima / Flora, Swaran Jeet Singh

Toxics

2022 Volume 10, Issue 12

Abstract: Copper (Cu), being an essential trace metal, plays several roles in biological processes, though exposure to Cu can be potentially toxic to the brain and a few other soft organs. In the present study, we investigated the effects of the combined ... ...

Abstract	Copper (Cu), being an essential trace metal, plays several roles in biological processes, though exposure to Cu can be potentially toxic to the brain and a few other soft organs. In the present study, we investigated the effects of the combined administration of monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA), which is a new chelator, and alpha lipoic acid (ALA) and an antioxidant that is made naturally in the body and is also found in foods, against Cu-induced oxidative stress in rats. Rats were exposed to 20 mg/kg copper sulfate for 16 weeks once a day via the oral route. After 16 weeks of exposure, animals were divided into different sub-groups. Group I was divided into three subgroups: Group IA, control; Group IB, MiADMSA (75 mg/kg, oral); Group IC, ALA (75 mg/kg, oral), while Group II was divided into four subgroups: Group IIA, Cu pre-exposed; Group IIB, Cu+ MiADMSA; Group IIC, Cu+ ALA; Group IID, Cu+ ALA+ MiADMSA. Exposure to Cu led to significant neurobehavioral abnormalities; treatment with MiADMSA, and in particular MiADMSA + ALA, significantly ameliorated the neurobehavioral parameters and restored the memory deficits in rats. Oxidative stress variables (ROS, nitrite, TBARS, SOD, catalase) and inflammatory markers (TNF-α, and IL-1β), which were altered on Cu exposed rats, also responded favorably to ALA+ MiADMSA combined treatment. Thus, combined administration of MiADMSA and ALA might be a better treatment strategy than monotherapy with MiADMSA or ALA against Cu-induced neurotoxicity, particularly in reducing oxidative stress, neurobehavioral abnormalities, and inflammatory markers.
Language	English
Publishing date	2022-11-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2733883-6
ISSN	2305-6304 ; 2305-6304
ISSN (online)	2305-6304
ISSN	2305-6304
DOI	10.3390/toxics10120718
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Article ; Online: Heavy Metal-Induced Cerebral Small Vessel Disease: Insights into Molecular Mechanisms and Possible Reversal Strategies.

Patwa, Jayant / Flora, Swaran Jeet Singh

International journal of molecular sciences

2020 Volume 21, Issue 11

Abstract: Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic ...

Abstract	Heavy metals are considered a continuous threat to humanity, as they cannot be eradicated. Prolonged exposure to heavy metals/metalloids in humans has been associated with several health risks, including neurodegeneration, vascular dysfunction, metabolic disorders, cancer, etc. Small blood vessels are highly vulnerable to heavy metals as they are directly exposed to the blood circulatory system, which has comparatively higher concentration of heavy metals than other organs. Cerebral small vessel disease (CSVD) is an umbrella term used to describe various pathological processes that affect the cerebral small blood vessels and is accepted as a primary contributor in associated disorders, such as dementia, cognitive disabilities, mood disorder, and ischemic, as well as a hemorrhagic stroke. In this review, we discuss the possible implication of heavy metals/metalloid exposure in CSVD and its associated disorders based on in-vitro, preclinical, and clinical evidences. We briefly discuss the CSVD, prevalence, epidemiology, and risk factors for development such as genetic, traditional, and environmental factors. Toxic effects of specific heavy metal/metalloid intoxication (As, Cd, Pb, Hg, and Cu) in the small vessel associated endothelium and vascular dysfunction too have been reviewed. An attempt has been made to highlight the possible molecular mechanism involved in the pathophysiology, such as oxidative stress, inflammatory pathway, matrix metalloproteinases (MMPs) expression, and amyloid angiopathy in the CSVD and related disorders. Finally, we discussed the role of cellular antioxidant defense enzymes to neutralize the toxic effect, and also highlighted the potential reversal strategies to combat heavy metal-induced vascular changes. In conclusion, heavy metals in small vessels are strongly associated with the development as well as the progression of CSVD. Chelation therapy may be an effective strategy to reduce the toxic metal load and the associated complications.
MeSH term(s)	Animals ; Antioxidants/therapeutic use ; Cerebral Small Vessel Diseases/chemically induced ; Cerebral Small Vessel Diseases/drug therapy ; Cerebral Small Vessel Diseases/metabolism ; Environmental Exposure/prevention & control ; Humans ; Metals, Heavy/toxicity
Chemical Substances	Antioxidants ; Metals, Heavy
Language	English
Publishing date	2020-05-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21113862
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Article ; Online: MiADMSA abrogates chronic copper-induced hepatic and immunological changes in Sprague Dawley rats.

Patwa, Jayant / Flora, S J S

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

2020 Volume 145, Page(s) 111692

Abstract: Wilson disease (WD) is an autosomal-recessive disorder associated with the impaired copper metabolism, resulting in hepatic and neurologic manifestations. D-Pencillamine (DPA) is a first-line of treatment however, monoisoamyl 2, 3-dimercaptosuccinic acid ...

Abstract	Wilson disease (WD) is an autosomal-recessive disorder associated with the impaired copper metabolism, resulting in hepatic and neurologic manifestations. D-Pencillamine (DPA) is a first-line of treatment however, monoisoamyl 2, 3-dimercaptosuccinic acid (MiADMSA), is gaining recognition recently as a future chelating agent of choice. We evaluated the effects of MiADMSA against copper-induced (20 mg/kg, orally, once, daily for 16 weeks) hepatic and immunological changes in the male Sprague Dawley (SD) rats. Copper overload increased the levels of pro-oxidant and concurrently decreased the levels of antioxidant enzymes in the liver. Increased oxidative stress triggered the up-regulation of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in the liver and down-regulated the anti-inflammatory cytokine IL-4. Altered liver function parameters as well as serum immunoglobulins' (IgG, IgA, IgE, and IgM) levels, were also noted. MiADMSA treatment restored most of copper altered biochemical and immunological changes. Further, the histopathological changes proved that MiADMSA treatment ameliorated copper induced hepatic injury. Infra red spectra of liver tissue indicated shift in the characteristic -OH peak during copper exposure while the shifting came to normal in MiADMSA administered rat liver. We conclude that MiADMSA could be a promising antidote for the chronic copper toxicity and possibly in the clinical management of WD.
MeSH term(s)	Animals ; Chelating Agents/administration & dosage ; Copper/adverse effects ; Cytokines/genetics ; Cytokines/immunology ; Hepatolenticular Degeneration/drug therapy ; Hepatolenticular Degeneration/genetics ; Hepatolenticular Degeneration/immunology ; Hepatolenticular Degeneration/pathology ; Humans ; Interleukin-1beta/genetics ; Interleukin-1beta/immunology ; Interleukin-6/genetics ; Interleukin-6/immunology ; Liver/drug effects ; Liver/immunology ; Liver/pathology ; Male ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley ; Succimer/administration & dosage
Chemical Substances	Chelating Agents ; Cytokines ; Interleukin-1beta ; Interleukin-6 ; Copper (789U1901C5) ; Succimer (DX1U2629QE)
Language	English
Publishing date	2020-08-29
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.2020.111692
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Article ; Online: Chemistry, Pharmacology, and Toxicology of Monoisoamyl Dimercaptosuccinic Acid: A Chelating Agent for Chronic Metal Poisoning.

Flora, Swaran J S / Jain, Keerti / Panghal, Archna / Patwa, Jayant

Chemical research in toxicology

2022 Volume 35, Issue 10, Page(s) 1701–1719

Abstract: Arsenic, a metalloid, is known to cause deleterious effects in various body organs, particularly the liver, urinary bladder, and brain, and these effects are primarily mediated through oxidative stress. Chelation therapy has been considered one of the ... ...

Abstract	Arsenic, a metalloid, is known to cause deleterious effects in various body organs, particularly the liver, urinary bladder, and brain, and these effects are primarily mediated through oxidative stress. Chelation therapy has been considered one of the promising medical treatments for arsenic poisoning. Meso 2,3- dimercaptosuccinic acid (DMSA) has been recognized as one of the most effective chelating drugs to treat arsenic poisoning. However, the drug is compromised with a number of shortcomings, including the inability to treat chronic arsenic poisoning due to its extracellular distribution. Monoisoamyl 2,3-dimercaptosuccinic acid, one of the analogues of meso 2,3-dimeraptosuccinic acid (DMSA), is a lipophilic chelator and has shown promise to be considered as a potential future chelating agent/antidote not only for arsenic but also for a few other heavy metals like lead, mercury, cadmium, and gallium arsenide. The results from numerous studies carried out in the recent past, mainly from our group, strongly support the clinical application of MiADMSA. This review paper summarizes most of the scientific details including the chemistry, pharmacology, and safety profile of MiADMSA. The efficacy of MiADMSA mainly against arsenic toxicity but also a few other heavy metals was also discussed. We also reviewed a few other strategies in order to achieve the optimum effects of MiADMSA, like combination therapy using two chelating agents or coadministration of a natural and synthetic antioxidant (including phytomedicine) along with MiADMSA for treatment of metal/metalloid poisoning. We also briefly discussed the use of nanotechnology (nano form of MiADMSA i.e. nano-MiADMSA) and compared it with bulk MiADMSA. All these strategies have been shown to be beneficial in getting more pronounced therapeutic efficacy of MiADMSA, as an adjuvant or as a complementary agent, by significantly increasing the chelating efficacy of MiADMSA.
MeSH term(s)	Animals ; Antidotes ; Antioxidants/therapeutic use ; Arsenic ; Arsenic Poisoning/drug therapy ; Cadmium ; Chelating Agents/pharmacology ; Chelating Agents/therapeutic use ; Heavy Metal Poisoning/drug therapy ; Mercury ; Rats ; Rats, Wistar ; Succimer/analogs & derivatives ; Succimer/pharmacology ; Succimer/therapeutic use
Chemical Substances	Antidotes ; Antioxidants ; Chelating Agents ; Cadmium (00BH33GNGH) ; monoisoamyl-2,3-dimercaptosuccinate (9O8B0VBE22) ; Succimer (DX1U2629QE) ; Mercury (FXS1BY2PGL) ; Arsenic (N712M78A8G)
Language	English
Publishing date	2022-08-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	639353-6
ISSN	1520-5010 ; 0893-228X
ISSN (online)	1520-5010
ISSN	0893-228X
DOI	10.1021/acs.chemrestox.2c00129
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Article ; Online: Melatonin ameliorates chronic copper-induced lung injury

Gaun, Sachin / Ali, Syed Afroz / Singh, Pooja / Patwa, Jayant / Flora, Swaran Jeet Singh / Datusalia, Ashok Kumar

Environ Sci Pollut Res. 2023 Feb., v. 30, no. 10 p.24949-24962

2023

Abstract: Copper (Cu) is an important trace element required for several biological processes. The use of copper is increasing gradually in several applications. Previous studies suggest that excess levels of copper are attributed to induce oxidative stress and ... ...

Abstract	Copper (Cu) is an important trace element required for several biological processes. The use of copper is increasing gradually in several applications. Previous studies suggest that excess levels of copper are attributed to induce oxidative stress and inflammation, mediating tissue damage. Inline, melatonin the hormone of darkness has been reported to exhibit various therapeutic effects including strong free radical scavenging properties and anti-inflammatory effects. However, its effects against pulmonary injury promoted by copper are not explored and remain unclear so far. Therefore, the present study was aimed to investigate the protective effect of melatonin against copper-induced lung damage. Female Sprague Dawley (SD) rats were exposed to 250 ppm of copper in drinking water for 16 weeks and treated with melatonin (i.p.) 5 and 10 mg/kg from the week (13–16th). The extent of tissue damage was assessed by tissue oxidative stress parameters, metal estimation and histological analysis. Copper-challenged rats showed altered oxidative stress variables. In addition, metal analysis revealed increased copper accumulation in the lungs and histological staining results further indicated severe tissue injury and inflammatory cell infiltration in copper-exposed rats. To this side, treatment with melatonin showed antioxidant and anti-inflammatory activities evidenced by reduced oxidative stress, tissue inflammation and collagen deposition as compared to copper-exposed animals. Moreover, spectral findings suggested melatonin treatment modulated the frequency sift, as compared to copper-challenged animals. Altogether, the present results suggest that melatonin might play a potential role in preventing copper-induced lung aberrations via inhibiting the ROS-mediated oxidative stress and inflammation.
Keywords	antioxidants ; collagen ; copper ; females ; free radicals ; histology ; inflammation ; lungs ; melatonin ; oxidative stress ; protective effect ; therapeutics
Language	English
Dates of publication	2023-02
Size	p. 24949-24962.
Publishing place	Springer Berlin Heidelberg
Document type	Article ; Online
ZDB-ID	1178791-0
ISSN	1614-7499 ; 0944-1344
ISSN (online)	1614-7499
ISSN	0944-1344
DOI	10.1007/s11356-022-19930-4
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Article ; Online: Nicotinamide attenuates cyclophosphamide-induced hepatotoxicity in SD rats by reducing oxidative stress and apoptosis.

Patwa, Jayant / Khan, Sabbir / Jena, Gopabandhu

Journal of biochemical and molecular toxicology

2020 Volume 34, Issue 10, Page(s) e22558

Abstract: Cyclophosphamide (CP) is a widely used anticancer and immunosuppressant drug. Nevertheless, clinical utilization of CP is limited due to considerable adverse effects and toxicities. Nicotinamide (NMD) is a micronutrient and the effect of NMD against CP- ... ...

Abstract	Cyclophosphamide (CP) is a widely used anticancer and immunosuppressant drug. Nevertheless, clinical utilization of CP is limited due to considerable adverse effects and toxicities. Nicotinamide (NMD) is a micronutrient and the effect of NMD against CP-induced hepatotoxicity is yet unexplored. The present study was designed to evaluate the chemoprotective effect of NMD against CP-induced hepatic injury in Sprague-Dawley rats. Hepatotoxicity was induced by the administration of CP (30 mg/kg/day) for 10 consecutive days by intraperitoneal injection. The chemoprotective effect of NMD treatment (200 mg/kg) against CP-induced hepatotoxicity was evaluated by the oxidative stress, liver function, histopathological changes, and DNA damage. NMD cotreatment significantly reduced CP-induced oxidative stress, histological changes, and apoptosis in the liver. The present study demonstrated that NMD treatment ameliorated CP-induced hepatic damage by improving the antioxidant system and reducing DNA damage. The present findings revealed that NMD supplementation might be useful to reduce CP-associated hepatotoxicity, and thereby can increase the therapeutic utility of CP.
MeSH term(s)	Animals ; Antineoplastic Agents, Alkylating/toxicity ; Apoptosis/drug effects ; Body Weight/drug effects ; Cyclophosphamide/toxicity ; Female ; Liver/drug effects ; Liver/enzymology ; Liver/metabolism ; Liver Function Tests ; Liver Glycogen/metabolism ; Niacinamide/pharmacology ; Organ Size/drug effects ; Oxidative Stress/drug effects ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Antineoplastic Agents, Alkylating ; Liver Glycogen ; Niacinamide (25X51I8RD4) ; Cyclophosphamide (8N3DW7272P)
Language	English
Publishing date	2020-07-01
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.22558
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Article ; Online: Synthesis, Molecular Docking, BSA, and

Thakur, Ashima / Patwa, Jayant / Sharma, Abha / Flora, Swaran Jeet Singh

Medicinal chemistry (Shariqah (United Arab Emirates))

2021 Volume 18, Issue 2, Page(s) 273–287

Abstract: Aim: To synthesize and evaluate the fused heterocyclic imidazo[1,2-a]pyridine based oxime as a reactivator against paraoxon inhibited acetylcholinesterase.: Background: Organophosphorus compounds (OPs) include parathion, malathion, chlorpyrifos, ... ...

Abstract	Aim: To synthesize and evaluate the fused heterocyclic imidazo[1,2-a]pyridine based oxime as a reactivator against paraoxon inhibited acetylcholinesterase. Background: Organophosphorus compounds (OPs) include parathion, malathion, chlorpyrifos, monocrotophos, and diazinon, which are commonly used in agriculture for enhancing agricultural productivity via killing crop-damaging pests. However, people may get exposed to OPs pesticides unintentionally/intentionally via ingestion, inhalation, or dermal. The current treatment regimen includes reactivator such as mono or bis-pyridinium oximes along with anticholinergic and anticonvulsant drugs that are recommended for the treatment of OP poisoning. Unfortunately, the drawback of the existing reactivator is the permanent charge present on the pyridinium, making them inefficient to cross the blood-brain barrier (BBB) and reactivate OP-inhibited central nervous system (CNS) acetylcholinesterase. Therefore, there is a need of a reactivator that could cross the BBB and reactivate the OP inhibited acetylcholinesterase. Objective: The objectives of the study were synthesis, molecular docking, BSA binding, and in-vitro estimation of oximes of various substituted imidazo [1,2-a]pyridine against paraoxon inhibited acetylcholinesterase. Methods: The reactivators were synthesized in three steps and characterized using various spectroscopic techniques. The molecular docking study was performed on 2WHP and 3ZLV PDB using the Glide-XP software. The acid dissociation constant (pKa) of oximes was calculated experimentally, and the drug-likeness properties of the oximes were calculated in silico using Molinspiration and Swiss ADME software. The binding of oximes with bovine serum albumin (BSA) was also investigated using a Fluorescence spectrophotometer. The reactivation potential of the oximes was determined by in vitro enzymatic assay. Results: The In-silico study inferred that the synthesized molecules fulfilled the parameters required for a successful CNS drug candidate. Furthermore, in-vitro enzymatic assay indicated reasonable reactivation potential of the oximes against paraoxon-inhibited AChE. The binding of oximes with bovine serum albumin (BSA) revealed that there was a static quenching of intrinsic fluorescence of BSA by the oxime. The binding constant value and number of binding sites were found to be 0.24 x 10 Conclusion: The results of the study concluded that this scaffold could be used for further designing of more efficient uncharged reactivators.
MeSH term(s)	Acetylcholinesterase ; Cholinesterase Reactivators/pharmacology ; Humans ; Imidazoles ; Molecular Docking Simulation ; Oximes/pharmacology ; Paraoxon/toxicity ; Pyridines ; Serum Albumin, Bovine
Chemical Substances	Cholinesterase Reactivators ; Imidazoles ; Oximes ; Pyridines ; imidazopyridine ; Serum Albumin, Bovine (27432CM55Q) ; Acetylcholinesterase (EC 3.1.1.7) ; Paraoxon (Q9CX8P80JW)
Language	English
Publishing date	2021-02-10
Publishing country	Netherlands
Document type	Journal Article
ISSN	1875-6638
ISSN (online)	1875-6638
DOI	10.2174/1573406417666210208223240
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Article ; Online: Synthesis and evaluation of small organic molecule as reactivator of organophosphorus inhibited acetylcholinesterase.

Thakur, Ashima / Patwa, Jayant / Pant, Suyash / Jeet Singh Flora, Swaran / Sharma, Abha

Drug and chemical toxicology

2022 Volume 47, Issue 1, Page(s) 26–41

Abstract: A series of uncharged salicylaldehyde oximes were synthesized and evaluated for the reactivation of organophosphorus (OP) nerve agents simulants Diethylchlorophosphonate (DCP) & Diethylcyanophosphonate (DCNP) and pesticides (paraoxon & malaoxon) ... ...

Abstract	A series of uncharged salicylaldehyde oximes were synthesized and evaluated for the reactivation of organophosphorus (OP) nerve agents simulants Diethylchlorophosphonate (DCP) & Diethylcyanophosphonate (DCNP) and pesticides (paraoxon & malaoxon) inhibited
MeSH term(s)	Cholinesterase Inhibitors/toxicity ; Cholinesterase Inhibitors/chemistry ; Paraoxon ; Cholinesterase Reactivators/pharmacology ; Cholinesterase Reactivators/chemistry ; Acetylcholinesterase/metabolism ; Molecular Docking Simulation ; Oximes/pharmacology ; Oximes/chemistry ; Organophosphorus Compounds/toxicity ; Malathion/analogs & derivatives ; Nitrophenols
Chemical Substances	Cholinesterase Inhibitors ; Paraoxon (Q9CX8P80JW) ; Cholinesterase Reactivators ; Acetylcholinesterase (EC 3.1.1.7) ; malaoxon (2439JYF84Q) ; 2,6-dichloro-4-nitrophenol (618-80-4) ; Oximes ; Organophosphorus Compounds ; Malathion (U5N7SU872W) ; Nitrophenols
Language	English
Publishing date	2022-12-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	548368-2
ISSN	1525-6014 ; 0148-0545
ISSN (online)	1525-6014
ISSN	0148-0545
DOI	10.1080/01480545.2022.2150210
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Article ; Online: Melatonin ameliorates chronic copper-induced lung injury.

Gaun, Sachin / Ali, Syed Afroz / Singh, Pooja / Patwa, Jayant / Flora, Swaran Jeet Singh / Datusalia, Ashok Kumar

Environmental science and pollution research international

2022 Volume 30, Issue 10, Page(s) 24949–24962

Abstract	Copper (Cu) is an important trace element required for several biological processes. The use of copper is increasing gradually in several applications. Previous studies suggest that excess levels of copper are attributed to induce oxidative stress and inflammation, mediating tissue damage. Inline, melatonin the hormone of darkness has been reported to exhibit various therapeutic effects including strong free radical scavenging properties and anti-inflammatory effects. However, its effects against pulmonary injury promoted by copper are not explored and remain unclear so far. Therefore, the present study was aimed to investigate the protective effect of melatonin against copper-induced lung damage. Female Sprague Dawley (SD) rats were exposed to 250 ppm of copper in drinking water for 16 weeks and treated with melatonin (i.p.) 5 and 10 mg/kg from the week (13-16th). The extent of tissue damage was assessed by tissue oxidative stress parameters, metal estimation and histological analysis. Copper-challenged rats showed altered oxidative stress variables. In addition, metal analysis revealed increased copper accumulation in the lungs and histological staining results further indicated severe tissue injury and inflammatory cell infiltration in copper-exposed rats. To this side, treatment with melatonin showed antioxidant and anti-inflammatory activities evidenced by reduced oxidative stress, tissue inflammation and collagen deposition as compared to copper-exposed animals. Moreover, spectral findings suggested melatonin treatment modulated the frequency sift, as compared to copper-challenged animals. Altogether, the present results suggest that melatonin might play a potential role in preventing copper-induced lung aberrations via inhibiting the ROS-mediated oxidative stress and inflammation.
MeSH term(s)	Rats ; Female ; Animals ; Melatonin/pharmacology ; Lung Injury/chemically induced ; Lung Injury/pathology ; Copper/toxicity ; Rats, Sprague-Dawley ; Antioxidants/metabolism ; Oxidative Stress ; Inflammation/drug therapy ; Lung ; Anti-Inflammatory Agents/pharmacology
Chemical Substances	Melatonin (JL5DK93RCL) ; Copper (789U1901C5) ; Antioxidants ; Anti-Inflammatory Agents
Language	English
Publishing date	2022-03-31
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/s11356-022-19930-4
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