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  1. Article ; Online: Increased Plasma Levels of Xanthurenic and Kynurenic Acids in Type 2 Diabetes.

    Oxenkrug, Gregory F

    Molecular neurobiology

    2015  Volume 52, Issue 2, Page(s) 805–810

    Abstract: About 350 million people worldwide have type 2 diabetes (T2D). The major risk factor of T2D is impaired glucose tolerance (pre-diabetes) with 10 % of pre-diabetes subjects develop T2D every year. Understanding of mechanisms of development of T2D from pre- ...

    Abstract About 350 million people worldwide have type 2 diabetes (T2D). The major risk factor of T2D is impaired glucose tolerance (pre-diabetes) with 10 % of pre-diabetes subjects develop T2D every year. Understanding of mechanisms of development of T2D from pre-diabetes is important for prevention and treatment of T2D. Chronic stress and chronic low-grade inflammation are prominent risk factors for T2D development in pre-diabetic subjects. However, molecular mechanisms mediating effect of stress and inflammation on development of T2D from pre-diabetes remain unknown. One of such mechanisms might involve kynurenine (KYN) pathway (KP) of tryptophan (TRP) metabolism. We suggested that chronic stress- or chronic low-grade inflammation-induced upregulation of formation of upstream KTP metabolites, KYN and 3-hydroxyKYN, combined with chronic stress- or chronic low-grade inflammation-induced deficiency of pyridoxal 5'-phosphate, a co-factor of downstream enzymes of KTP, triggers overproduction of diabetogenic downstream KYN metabolites, kynurenic acid (KYNA) and 3-hydroxyKYNA (also known as xanthurenic acid (XA)). As the initial assessment of our working hypothesis, we evaluated plasma levels of up- and downstream KP metabolites in the same samples of T2D patients. KYN, XA, and KYNA levels in plasma samples of T2D patients were higher than in samples of non-diabetic subjects. Our results provide further support of "kynurenine hypothesis of insulin resistance and its progression to T2D" that suggested that overproduction of diabetogenic KP metabolites, induced by chronic stress or chronic low-grade inflammation, is one of the mechanisms promoting development of T2D from pre-diabetes. Downstream metabolites of KP might serve as biomarkers of T2D and targets for clinical intervention.
    MeSH term(s) 3-Hydroxyanthranilic Acid/metabolism ; Adult ; Aged ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/drug therapy ; Female ; Humans ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Inflammation/blood ; Kynurenic Acid/blood ; Kynurenine/metabolism ; Male ; Metformin/pharmacology ; Metformin/therapeutic use ; Middle Aged ; Prediabetic State/blood ; Pyridoxal Phosphate/physiology ; Stress, Physiological ; Tryptophan/metabolism ; Tryptophan Oxygenase/metabolism ; Xanthurenates/blood
    Chemical Substances Hypoglycemic Agents ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Xanthurenates ; 3-Hydroxyanthranilic Acid (1UQB1BT4OT) ; Kynurenine (343-65-7) ; xanthurenic acid (58LAB1BG8J) ; Pyridoxal Phosphate (5V5IOJ8338) ; Tryptophan (8DUH1N11BX) ; Metformin (9100L32L2N) ; Tryptophan Oxygenase (EC 1.13.11.11) ; Kynurenic Acid (H030S2S85J)
    Language English
    Publishing date 2015-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-015-9232-0
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  2. Article ; Online: Kynurenine and hypotension: historic perspectives.

    Oxenkrug, Gregory F

    Critical care medicine

    2012  Volume 40, Issue 6, Page(s) 2006; author reply 2006–7

    MeSH term(s) Female ; Humans ; Hypotension/etiology ; Kynurenine/biosynthesis ; Male ; Shock, Septic/complications ; Tryptophan/metabolism
    Chemical Substances Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX)
    Language English
    Publishing date 2012-06
    Publishing country United States
    Document type Comment ; Letter
    ZDB-ID 197890-1
    ISSN 1530-0293 ; 0090-3493
    ISSN (online) 1530-0293
    ISSN 0090-3493
    DOI 10.1097/CCM.0b013e31824e1e3b
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  3. Article ; Online: Tryptophan kynurenine metabolism as a common mediator of genetic and environmental impacts in major depressive disorder: the serotonin hypothesis revisited 40 years later.

    Oxenkrug, Gregory F

    The Israel journal of psychiatry and related sciences

    2010  Volume 47, Issue 1, Page(s) 56–63

    Abstract: The original 1969 Lancet paper proposed in depression the activity of liver tryptophan-pyrrolase is stimulated by raised blood corticosteroids levels, and metabolism of tryptophan is shunted away from serotonin production, and towards kynurenine ... ...

    Abstract The original 1969 Lancet paper proposed in depression the activity of liver tryptophan-pyrrolase is stimulated by raised blood corticosteroids levels, and metabolism of tryptophan is shunted away from serotonin production, and towards kynurenine production. Discovery of neurotropic activity of kynurenines suggested that up-regulation of the tryptophan-kynurenine pathway not only augmented serotonin deficiency but also underlined depression-associated anxiety, psychosis and cognitive decline. The present review of genetic and hormonal factors regulating kynurenine pathway of tryptophan metabolism suggests that this pathway mediates both genetic and environmental mechanisms of depression. Rate-limiting enzymes of kynurenine formation, tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO) are activated by stress hormones (TDO) and/or by pro-inflammatory cytokines (IDO). Simultaneous presence of high producers alleles of proinflammatory cytokines genes (e.g., interferon-gamma and tumor necrosis factor-alpha) determines the genetic predisposition to depression via up-regulation of IDO while impact of environmental stresses is mediated via hormonal activation of TDO. Tryptophan-kynurenine pathway represents a major meeting point of gene-environment interaction in depression and a new target for pharmacological intervention.
    MeSH term(s) Adrenal Cortex Hormones/metabolism ; Animals ; Biosynthetic Pathways/genetics ; Cytokines/genetics ; Cytokines/metabolism ; Depressive Disorder, Major/genetics ; Depressive Disorder, Major/metabolism ; Environment ; Genetic Predisposition to Disease ; Humans ; Indoleamine-Pyrrole 2,3,-Dioxygenase/genetics ; Indoleamine-Pyrrole 2,3,-Dioxygenase/metabolism ; Interferon-gamma/metabolism ; Kynurenine/metabolism ; Serotonin/deficiency ; Stress, Psychological/metabolism ; Tryptophan/metabolism ; Tryptophan Oxygenase/genetics ; Tryptophan Oxygenase/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation/genetics
    Chemical Substances Adrenal Cortex Hormones ; Cytokines ; Indoleamine-Pyrrole 2,3,-Dioxygenase ; Tumor Necrosis Factor-alpha ; Serotonin (333DO1RDJY) ; Kynurenine (343-65-7) ; Interferon-gamma (82115-62-6) ; Tryptophan (8DUH1N11BX) ; Tryptophan Oxygenase (EC 1.13.11.11)
    Language English
    Publishing date 2010-08-06
    Publishing country Israel
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 604431-1
    ISSN 2617-2402 ; 0333-7308
    ISSN (online) 2617-2402
    ISSN 0333-7308
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  4. Article ; Online: Metabolic syndrome, age-associated neuroendocrine disorders, and dysregulation of tryptophan-kynurenine metabolism.

    Oxenkrug, Gregory F

    Annals of the New York Academy of Sciences

    2010  Volume 1199, Page(s) 1–14

    Abstract: The neuroendocrine theory of aging identified a cluster of conditions (hypertension, obesity, dyslipidemia, diabetes type 2, menopause, late onset depression, vascular cognitive impairment, impairment of immune defense, and some forms of cancer, e.g., ... ...

    Abstract The neuroendocrine theory of aging identified a cluster of conditions (hypertension, obesity, dyslipidemia, diabetes type 2, menopause, late onset depression, vascular cognitive impairment, impairment of immune defense, and some forms of cancer, e.g., breast and prostate) as age-associated neuroendocrine disorders (AAND). Obesity, dyslipidemia, hypertension, and type 2 diabetes were later described as metabolic syndromes (MetS). Chronic inflammation is currently considered as a common feature of MetS/AAND. One of the mechanisms by which chronic inflammation might trigger and/or maintain the development of MetS/AAND is transcriptional induction of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of tryptophan (TRY)-kynurenine (KYN) pathway, by pro-inflammatory cytokines (PIC). Activation of IDO shifts TRY metabolism from serotonin synthesis to formation of "kynurenines." Diminished serotonin production is associated with mental depression while increased formation of kynurenines might contribute to development of MetS/AAND via their apoptotic, neurotoxic, and pro-oxidative effects, and upregulation of inducible nitric oxide synthase, phospholipase A2, arachidonic acid, prostaglandin, 5-lipoxygenase, and leukotriene cascade. The combined presence of high producers of alleles of polymorphic PIC genes (e.g., interferon-gamma and tumor necrosis factor alpha) might account for the genetic predisposition to high levels of PIC production, leading to "superinduction" of IDO. The other rate-limiting enzyme of the TRY-KYN pathway, TRY 2,3-dioxygenase, is activated by substrate (TRY) and cortisol. Therefore, KYN-TRY metabolism might be the meeting point for gene-environment interaction and a new target for prevention and treatment of MetS/AAND.
    MeSH term(s) Aging/metabolism ; Animals ; Endocrine System Diseases/complications ; Endocrine System Diseases/metabolism ; Endocrine System Diseases/physiopathology ; Humans ; Kynurenine/metabolism ; Metabolic Syndrome/complications ; Metabolic Syndrome/metabolism ; Metabolic Syndrome/physiopathology ; Nervous System Diseases/complications ; Nervous System Diseases/metabolism ; Nervous System Diseases/physiopathology ; Tryptophan/metabolism
    Chemical Substances Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX)
    Language English
    Publishing date 2010-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/j.1749-6632.2009.05356.x
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  5. Article ; Online: Interferon-gamma-inducible kynurenines/pteridines inflammation cascade: implications for aging and aging-associated psychiatric and medical disorders.

    Oxenkrug, Gregory F

    Journal of neural transmission (Vienna, Austria : 1996)

    2010  Volume 118, Issue 1, Page(s) 75–85

    Abstract: This review of literature and our data suggests that up-regulated production of interferon-gamma (IFNG) in periphery and brain triggers a merger of tryptophan (TRY)-kynurenine (KYN) and guanine-tetrahydrobiopterin (BH4) metabolic pathways into ... ...

    Abstract This review of literature and our data suggests that up-regulated production of interferon-gamma (IFNG) in periphery and brain triggers a merger of tryptophan (TRY)-kynurenine (KYN) and guanine-tetrahydrobiopterin (BH4) metabolic pathways into inflammation cascade involved in aging and aging-associated medical and psychiatric disorders (AAMPD) (metabolic syndrome, depression, vascular cognitive impairment). IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production. Superoxide anion and free radicals among KYN derivatives trigger phospholipase A2-arachidonic acid cascade associated with AAMPD. IFNG-induced up-regulation of indoleamine 2,3-dioxygenase (IDO), rate-limiting enzyme of TRY-KYN pathway, decreases TRY conversion into serotonin (substrate of antidepressant effect) and increases production of KYN associated with diabetes [xanthurenic acid (XA)], anxiety (KYN), psychoses and cognitive impairment (kynurenic acid). IFNG-inducible KYN/pteridines inflammation cascade is impacted by IFNG (+874) T/A genotypes, encoding cytokine production. In addition to literature data on KYN/TRY ratio (IDO activity index), we observe neopterin levels (index of activity of rate-limiting enzyme of guanine-BH4 pathway) to be higher in carriers of high (T) than of low (A) producers alleles; and to correlate with AAMPD markers (e.g., insulin resistance, body mass index, mortality risk), and with IFN-alpha-induced depression in hepatitis C patients. IFNG-inducible cascade is influenced by environmental factors (e.g., vitamin B6 deficiency increases XA formation) and by pharmacological agents; and might offer new approaches for anti-aging and anti-AAMPD interventions.
    MeSH term(s) Aging/genetics ; Aging/physiology ; Animals ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Interferon-gamma/pharmacology ; Kynurenine/metabolism ; Kynurenine/physiology ; Mental Disorders/genetics ; Mental Disorders/pathology ; Metabolic Syndrome/genetics ; Metabolic Syndrome/metabolism ; Obesity/genetics ; Obesity/pathology ; Polymorphism, Genetic/genetics ; Pteridines/metabolism ; Signal Transduction/drug effects
    Chemical Substances Pteridines ; Kynurenine (343-65-7) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2010-09-02
    Publishing country Austria
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-010-0475-7
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  6. Article ; Online: The extended life span of Drosophila melanogaster eye-color (white and vermilion) mutants with impaired formation of kynurenine.

    Oxenkrug, Gregory F

    Journal of neural transmission (Vienna, Austria : 1996)

    2009  Volume 117, Issue 1, Page(s) 23–26

    Abstract: Animal and human studies suggest that aging is associated with increased formation of kynurenine (KYN) from tryptophan (TRY). The rate-limiting factors of TRY-KYN metabolism are transmembrane transport of TRY, and activity of enzyme, TRY 2,3-dioxygenase ( ...

    Abstract Animal and human studies suggest that aging is associated with increased formation of kynurenine (KYN) from tryptophan (TRY). The rate-limiting factors of TRY-KYN metabolism are transmembrane transport of TRY, and activity of enzyme, TRY 2,3-dioxygenase (TDO2). Eye-color mutants, white (w1118) (impaired TRY transport) and vermilion (v48a and v2) (deficient TDO activity), were compared with wild-type Oregon-R (Ore-R) strain of Drosophila melanogaster. Female 1-day-old adult flies maintained on a standard medium, and acclimatized to 12-h light:12-h dark cycle were collected, and then regularly transferred to fresh medium every 3-4 days. The number of dead flies was recorded at the time of transfer. Forty flies were studied in each experimental group. The life span of w1118 (mean = 45.5 days), and v48a (mean = 47.6 days) and v2 (mean = 43.8 days), were significantly longer than of wild-type Ore-R flies (27.1 days) (p < 0.001, Logrank test). There were no differences in life span between w1118 and v48a and v2 mutants. Present results suggest that prolongation of life span may be associated with slow rate of KYN formation from TRY.
    MeSH term(s) Animals ; Animals, Genetically Modified ; Biological Transport, Active/genetics ; Drosophila melanogaster ; Eye ; Female ; Kynurenine/genetics ; Kynurenine/metabolism ; Longevity/genetics ; Mutation ; Pigmentation/genetics ; Species Specificity ; Time Factors ; Tryptophan/metabolism ; Tryptophan Oxygenase/genetics
    Chemical Substances Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX) ; Tryptophan Oxygenase (EC 1.13.11.11)
    Language English
    Publishing date 2009-11-26
    Publishing country Austria
    Document type Journal Article
    ZDB-ID 184163-4
    ISSN 1435-1463 ; 0300-9564
    ISSN (online) 1435-1463
    ISSN 0300-9564
    DOI 10.1007/s00702-009-0341-7
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  7. Article: Genetic and hormonal regulation of tryptophan kynurenine metabolism: implications for vascular cognitive impairment, major depressive disorder, and aging.

    Oxenkrug, Gregory F

    Annals of the New York Academy of Sciences

    2007  Volume 1122, Page(s) 35–49

    Abstract: Impairment of cognition that is caused by (or associated with) vascular factors has been termed vascular cognitive impairment (VCI). The hallmark of VCI is an impairment of brain executive, or planning, functions caused by inflammatory changes of brain ... ...

    Abstract Impairment of cognition that is caused by (or associated with) vascular factors has been termed vascular cognitive impairment (VCI). The hallmark of VCI is an impairment of brain executive, or planning, functions caused by inflammatory changes of brain microvessels. VCI is characterized by impairment of the executive function and is distinct from Alzheimer's-type and multi-infarct dementias, although VCI might overlap with Alzheimer's disease. This review focuses on the possible contribution of the kynurenine pathway of tryptophan (Try) catabolism to the inflammatory changes in brain microvessels. One mechanism of brain microvessel inflammation is activation of the inducible nitric oxide synthase (iNOS) by the proinflammatory cytokine interferon gamma (IFN-gamma). The effect of IFN-gamma on iNOS might be mediated by kynurenine derivatives of tryptophan because (1) IFN-gamma stimulates the rate-determining enzyme of the Try-kynurenine pathway, indoleamine-2,3-dioxygenase (IDO) and (2) some kynurenines (e.g., quinolinic and picolinic acids) can stimulate iNOS. IFN-gamma production is controlled by (IFN-gamma) + 874(T/A) genotypes, suggesting the association of a high promoter T allele with the high rate of IFN-gamma production and, consequently, with activated IDO and enhanced production of kynurenines. Although IDO is strictly an IFN-gamma-induced gene product, tumor necrosis factor alpha (TNF-alpha) can synergistically increase the transcriptional activation of the IDO gene in response to IFN-gamma. The combination of high promoter T of (IFN-gamma) + 874(T/A) with high promoter A of (TNF-alpha) -308(G/A) might "superinduce" IDO and cause (or contribute to) inflammation of brain microvessels detected as white matter hyperintensities and leading to VCI development. Hormonal induction of tryptophan dioxygenase and the ability of hormones to potentiate IFN-gamma-induced activation of IDO might contribute to the development of inflammatory changes in major depressive disorder and in aging. The IFN-gamma-IDO-iNOS hypothesis of VCI suggests new ways of preventing (identifying population at risk by analysis of IFN-gamma and TNF-alpha genetic polymorphism) and treating VCI (using IDO inhibitors and melatonin and bupropion [Wellbutrin] as agents suppressing IFN-gamma and TNF-alpha production).
    MeSH term(s) Aging/genetics ; Aging/metabolism ; Animals ; Cognition Disorders/genetics ; Cognition Disorders/metabolism ; Cytokines/genetics ; Cytokines/metabolism ; Depressive Disorder, Major/genetics ; Depressive Disorder, Major/metabolism ; Hormones/physiology ; Humans ; Kynurenine/genetics ; Kynurenine/metabolism ; Models, Biological ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Tryptophan/genetics ; Tryptophan/metabolism
    Chemical Substances Cytokines ; Hormones ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
    Language English
    Publishing date 2007-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1196/annals.1403.003
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  8. Article: Plasma Anthranilic Acid and Leptin Levels Predict HAM-D Scores in Depressed Women.

    Steiner, Johann / Dobrowolny, Henrik / Guest, Paul C / Bernstein, Hans-Gert / Fuchs, Dietmar / Roeser, Julien / Summergrad, Paul / Oxenkrug, Gregory F

    International journal of tryptophan research : IJTR

    2021  Volume 14, Page(s) 11786469211016474

    Abstract: Objectives: Major depressive disorder (MDD) is associated with dysregulations of leptin and tryptophan-kynurenine (Trp-Kyn) (TKP) pathways. Leptin, a pro-inflammatory cytokine, activates Trp conversion into Kyn. However, leptin association with down- ... ...

    Abstract Objectives: Major depressive disorder (MDD) is associated with dysregulations of leptin and tryptophan-kynurenine (Trp-Kyn) (TKP) pathways. Leptin, a pro-inflammatory cytokine, activates Trp conversion into Kyn. However, leptin association with down-stream Kyn metabolites in MDD is unknown.
    Methods: Fasting plasma samples from 29 acutely ill drug-naïve (n = 16) or currently non-medicated (⩾6 weeks; n = 13) MDD patients were analyzed for leptin, Trp, Kyn, its down-stream metabolites (anthranilic [AA], kynurenic [KYNA], xanthurenic [XA] acids and 3-hydroxykynurenine [3HK]), C-reactive protein (CRP), neopterin, body mass index (BMI), and insulin resistance (HOMA-IR). Depression severity was assessed by HAM-D-21.
    Results: In female (n = 14) (but not in male) patients HAM-D-21 scores correlated with plasma levels of AA (but not other Kyn metabolites) (rho = -0.644,
    Conclusions: Present findings of gender specific AA/Leptin correlations with HAM-D are important considering that AA and leptin are transported from plasma into brain, and that AA formation is catalyzed by
    Language English
    Publishing date 2021-05-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2517435-6
    ISSN 1178-6469
    ISSN 1178-6469
    DOI 10.1177/11786469211016474
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  9. Article ; Online: Ramelteon attenuates age-associated hypertension and weight gain in spontaneously hypertensive rats.

    Oxenkrug, Gregory F / Summergrad, Paul

    Annals of the New York Academy of Sciences

    2010  Volume 1199, Page(s) 114–120

    Abstract: The neuroendocrine theory of aging suggests the common mechanisms of developmental (prereproductive) and aging (postreproductive) processes and identified a cluster of conditions (hypertension, obesity, dyslipidemia, type 2 diabetes, menopause, late ... ...

    Abstract The neuroendocrine theory of aging suggests the common mechanisms of developmental (prereproductive) and aging (postreproductive) processes and identified a cluster of conditions (hypertension, obesity, dyslipidemia, type 2 diabetes, menopause, late onset depression, vascular cognitive impairment, impairment of immune defense, and some forms of cancer) as age-associated neuroendocrine disorders (AAND). Obesity, dyslipidemia, hypertension, and type 2 diabetes were later described as metabolic syndrome (MetS). Because melatonin attenuated development of MetS is age-dependent, that is, in young and old, but not in middle-aged rats, we studied the effect of the selective melatonin agonist, Ramelteon, on the two core symptoms of MetS/AAND: hypertension and body weight gain in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto male rats (WKY). SHR rats developed hypertension at the time of maximal weight gain that coincided with the onset of reproductive activity (8-10 weeks old). Chronic (but not acute) administration of Ramelteon (in drinking water, 8 mg/kg/day, from 4 to 12 weeks of age) attenuated age-associated increase of systolic blood pressure (tail-cuff method) by 45%, and age-associated body weight gain by 30%. Acute and chronic Ramelteon did not affect blood pressure and body weight in normotensive WKY rats. Ramelteon-induced attenuation of age-associated hypertension and weight gain suggests that Ramelteon might attenuate the other symptoms of MetS/AAND and might be useful in the treatment of MetS/AAND during puberty, menopause, and old age.
    MeSH term(s) Animals ; Hypertension/drug therapy ; Hypertension/physiopathology ; Indenes/pharmacology ; Indenes/therapeutic use ; Male ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Weight Gain/drug effects
    Chemical Substances Indenes ; ramelteon (901AS54I69)
    Language English
    Publishing date 2010-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/j.1749-6632.2009.05355.x
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  10. Article: Effect of luzindole and other melatonin receptor antagonists on iron- and lipopolysaccharide-induced lipid peroxidation in vitro.

    Requintina, Pura J / Oxenkrug, Gregory F

    Annals of the New York Academy of Sciences

    2007  Volume 1122, Page(s) 289–294

    Abstract: Melatonin and its precursor, N-acetylserotonin (NAS), have been shown in in vivo and in vitro studies to inhibit iron- and lipopolysaccharide (LPS)-induced lipid peroxidation in rats and mice. Using in vitro studies, we examined whether these effects ... ...

    Abstract Melatonin and its precursor, N-acetylserotonin (NAS), have been shown in in vivo and in vitro studies to inhibit iron- and lipopolysaccharide (LPS)-induced lipid peroxidation in rats and mice. Using in vitro studies, we examined whether these effects will be affected by the melatonin receptor antagonists luzindole (a competitive MT(1)/MT(2) antagonist), DH 97 (MT(2)), prazosin (MT(3)), and 4-P-PDOT (MT(2)). Lipid peroxidation in the form of malondialdehyde (MDA) was assayed by measuring thiobarbituric acid-reactive substances. The antagonists did not affect the melatonin and NAS effect on iron- and LPS-induced peroxidation. However, luzindole alone, but not the other antagonists, inhibited the iron- and LPS-induced peroxidation in the rat brain and kidney homogenates. At a dose of 50 microM, luzindole reduced iron-induced MDA levels by 80% in the brain and 84% in the kidney, whereas LPS-induced MDA levels were reduced by 85% in both brain and kidney. A dose of 800 microM prevented lipid peroxidation, bringing the MDA levels to values of samples untreated by iron or LPS.
    MeSH term(s) Animals ; Brain/drug effects ; Brain/metabolism ; Brain Chemistry/drug effects ; Dose-Response Relationship, Drug ; Drug Interactions ; In Vitro Techniques ; Iron/pharmacology ; Kidney/drug effects ; Kidney/metabolism ; Lipid Peroxidation/drug effects ; Lipopolysaccharides/pharmacology ; Male ; Rats ; Rats, Inbred F344 ; Receptors, Melatonin/antagonists & inhibitors ; Thiobarbituric Acid Reactive Substances/metabolism ; Tryptamines/pharmacology
    Chemical Substances Lipopolysaccharides ; Receptors, Melatonin ; Thiobarbituric Acid Reactive Substances ; Tryptamines ; luzindole (117946-91-5) ; Iron (E1UOL152H7)
    Language English
    Publishing date 2007-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1196/annals.1403.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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