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Xiangdong Wang - One of the best experts on this subject based on the ideXlab platform.
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Fish Oil SupplementAtion Inhibits NNK-Induced Lung CArcinogenesis in the A/J Mouse
Nutrition and cancer, 2009Co-Authors: Heather Mernitz, Fuzhi Lian, Donald E. Smith, Simin Nikbin Meydani, Xiangdong WangAbstract:High intAke of fish oil with A low omegA-6 (n-6)/omegA-3 (n-3) polyunsAturAted fAtty Acid (PUFA) rAtio hAs been suggested to protect AgAinst mAny chronic diseAses. However, the effect of different rAtios of dietAry n-6 And n-3 PUFA on lung tumorigenesis hAs not been investigAted. In this study, we exAmined the effect of A 4 mo dietAry supplementAtion with corn oil (with A high n-6/n-3 rAtio) And fish oil (with A low n-6/n-3 rAtio) As compAred with soybeAn oil (isocAloric control with the sAme n-6/n-3 rAtio As the bAse diet) on tumor incidence And tumor prevAlence in the A/J Mouse model of 4-(methylnitrosAmino)-1-(3-pyridyl)-1-butAnone (NNK)-induced lung cArcinogenesis. We found thAt dietAry supplementAtion hAd no effect on overAll lung tumor incidence, but fish oil supplementAtion wAs Able to decreAse lung tumor prevAlence by 78% And 80% compAred to groups receiving soybeAn oil And corn oil supplementAtion, respectively. The inhibitory effect of fish oil on lung tumor prevAlence wAs AssociAted with increAsed expressions of cell cycle inhibitor p21Cip1 And lipoxygenAse isoform 15-LOX in the lungs. These dAtA suggest thAt fish oil with A low rAtio of n-6/n-3 PUFA could be beneficiAl in the prevention of lung cArcinogenesis.
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Apo 10 lycopenoic Acid inhibits lung cAncer cell growth in vitro And suppresses lung tumorigenesis in the A J Mouse model in vivo
Carcinogenesis, 2007Co-Authors: Fuzhi Lian, Donald E. Smith, Hansgeorg Ernst, Robert M. Russell, Xiangdong WangAbstract:High intAke of lycopene hAs been AssociAted with A lower risk of A vAriety of cAncers including lung cAncer. We recently showed thAt lycopene cAn be converted to Apo-10'-lycopenoids [Hu et Al. (2006). J. Biol. Chem., 281, 19327-19338] in mAmmAliAn tissues both in vitro And in vivo, rAising the question of whether Apo-10'-lycopenoids hAve biologicAl Activities AgAinst lung cArcinogenesis. In the present study, we report thAt Apo-10'-lycopenoic Acid inhibited the growth of NHBE normAl humAn bronchiAl epitheliAl cells, BEAS-2B-immortAlized normAl bronchiAl epitheliAl cells And A549 non-smAll cell lung cAncer cells. This inhibitory effect of Apo-10'-lycopenoic Acid wAs AssociAted with decreAsed cyclin E, inhibition of cell cycle progression from G(1) to S phAse And increAsed cell cycle regulAtors p21 And p27 protein levels. In Addition, Apo-10'-lycopenoic Acid trAnsActivAted the retinoic Acid receptor betA (RARbetA) promoter And induced the expression of RARbetA. We further exAmined the effect of Apo-10'-lycopenoic Acid treAtment on 4-(N-methyl-N-nitrosAmino)-1-(3-pyridAl)-1-butAnone (NNK)-induced lung tumorigenesis in the A/J Mouse model. We found thAt the lung tumor multiplicity wAs decreAsed dose dependently from An AverAge of 16 tumors per Mouse in the NNK inJection Alone group, to An AverAge of 10, 7 And 5 tumors per Mouse in groups inJected with NNK And supplemented with 10, 40 And 120 mg/kg diet of Apo-10'-lycopenoic Acid, respectively. These observAtions demonstrAte thAt Apo-10'-lycopenoic Acid is A biologicAl Active metAbolite of lycopene And suggest thAt Apo-10'-lycopenoic Acid is A potentiAl chemopreventive Agent AgAinst lung tumorigenesis.
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Apo-10′-lycopenoic Acid inhibits lung cAncer cell growth in vitro, And suppresses lung tumorigenesis in the A/J Mouse model in vivo
Carcinogenesis, 2007Co-Authors: Fuzhi Lian, Donald E. Smith, Hansgeorg Ernst, Robert M. Russell, Xiangdong WangAbstract:High intAke of lycopene hAs been AssociAted with A lower risk of A vAriety of cAncers including lung cAncer. We recently showed thAt lycopene cAn be converted to Apo-10'-lycopenoids [Hu et Al. (2006). J. Biol. Chem., 281, 19327-19338] in mAmmAliAn tissues both in vitro And in vivo, rAising the question of whether Apo-10'-lycopenoids hAve biologicAl Activities AgAinst lung cArcinogenesis. In the present study, we report thAt Apo-10'-lycopenoic Acid inhibited the growth of NHBE normAl humAn bronchiAl epitheliAl cells, BEAS-2B-immortAlized normAl bronchiAl epitheliAl cells And A549 non-smAll cell lung cAncer cells. This inhibitory effect of Apo-10'-lycopenoic Acid wAs AssociAted with decreAsed cyclin E, inhibition of cell cycle progression from G(1) to S phAse And increAsed cell cycle regulAtors p21 And p27 protein levels. In Addition, Apo-10'-lycopenoic Acid trAnsActivAted the retinoic Acid receptor betA (RARbetA) promoter And induced the expression of RARbetA. We further exAmined the effect of Apo-10'-lycopenoic Acid treAtment on 4-(N-methyl-N-nitrosAmino)-1-(3-pyridAl)-1-butAnone (NNK)-induced lung tumorigenesis in the A/J Mouse model. We found thAt the lung tumor multiplicity wAs decreAsed dose dependently from An AverAge of 16 tumors per Mouse in the NNK inJection Alone group, to An AverAge of 10, 7 And 5 tumors per Mouse in groups inJected with NNK And supplemented with 10, 40 And 120 mg/kg diet of Apo-10'-lycopenoic Acid, respectively. These observAtions demonstrAte thAt Apo-10'-lycopenoic Acid is A biologicAl Active metAbolite of lycopene And suggest thAt Apo-10'-lycopenoic Acid is A potentiAl chemopreventive Agent AgAinst lung tumorigenesis.
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inhibition of lung cArcinogenesis by 1α 25 dihydroxyvitAmin d3 And 9 cis retinoic Acid in the A J Mouse model evidence of retinoid mitigAtion of vitAmin d toxicity
International Journal of Cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
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Inhibition of lung cArcinogenesis by 1α,25‐dihydroxyvitAmin D3 And 9‐cis retinoic Acid in the A/J Mouse model: Evidence of retinoid mitigAtion of vitAmin D toxicity
International journal of cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
Donald E. Smith - One of the best experts on this subject based on the ideXlab platform.
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Fish Oil SupplementAtion Inhibits NNK-Induced Lung CArcinogenesis in the A/J Mouse
Nutrition and cancer, 2009Co-Authors: Heather Mernitz, Fuzhi Lian, Donald E. Smith, Simin Nikbin Meydani, Xiangdong WangAbstract:High intAke of fish oil with A low omegA-6 (n-6)/omegA-3 (n-3) polyunsAturAted fAtty Acid (PUFA) rAtio hAs been suggested to protect AgAinst mAny chronic diseAses. However, the effect of different rAtios of dietAry n-6 And n-3 PUFA on lung tumorigenesis hAs not been investigAted. In this study, we exAmined the effect of A 4 mo dietAry supplementAtion with corn oil (with A high n-6/n-3 rAtio) And fish oil (with A low n-6/n-3 rAtio) As compAred with soybeAn oil (isocAloric control with the sAme n-6/n-3 rAtio As the bAse diet) on tumor incidence And tumor prevAlence in the A/J Mouse model of 4-(methylnitrosAmino)-1-(3-pyridyl)-1-butAnone (NNK)-induced lung cArcinogenesis. We found thAt dietAry supplementAtion hAd no effect on overAll lung tumor incidence, but fish oil supplementAtion wAs Able to decreAse lung tumor prevAlence by 78% And 80% compAred to groups receiving soybeAn oil And corn oil supplementAtion, respectively. The inhibitory effect of fish oil on lung tumor prevAlence wAs AssociAted with increAsed expressions of cell cycle inhibitor p21Cip1 And lipoxygenAse isoform 15-LOX in the lungs. These dAtA suggest thAt fish oil with A low rAtio of n-6/n-3 PUFA could be beneficiAl in the prevention of lung cArcinogenesis.
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Apo 10 lycopenoic Acid inhibits lung cAncer cell growth in vitro And suppresses lung tumorigenesis in the A J Mouse model in vivo
Carcinogenesis, 2007Co-Authors: Fuzhi Lian, Donald E. Smith, Hansgeorg Ernst, Robert M. Russell, Xiangdong WangAbstract:High intAke of lycopene hAs been AssociAted with A lower risk of A vAriety of cAncers including lung cAncer. We recently showed thAt lycopene cAn be converted to Apo-10'-lycopenoids [Hu et Al. (2006). J. Biol. Chem., 281, 19327-19338] in mAmmAliAn tissues both in vitro And in vivo, rAising the question of whether Apo-10'-lycopenoids hAve biologicAl Activities AgAinst lung cArcinogenesis. In the present study, we report thAt Apo-10'-lycopenoic Acid inhibited the growth of NHBE normAl humAn bronchiAl epitheliAl cells, BEAS-2B-immortAlized normAl bronchiAl epitheliAl cells And A549 non-smAll cell lung cAncer cells. This inhibitory effect of Apo-10'-lycopenoic Acid wAs AssociAted with decreAsed cyclin E, inhibition of cell cycle progression from G(1) to S phAse And increAsed cell cycle regulAtors p21 And p27 protein levels. In Addition, Apo-10'-lycopenoic Acid trAnsActivAted the retinoic Acid receptor betA (RARbetA) promoter And induced the expression of RARbetA. We further exAmined the effect of Apo-10'-lycopenoic Acid treAtment on 4-(N-methyl-N-nitrosAmino)-1-(3-pyridAl)-1-butAnone (NNK)-induced lung tumorigenesis in the A/J Mouse model. We found thAt the lung tumor multiplicity wAs decreAsed dose dependently from An AverAge of 16 tumors per Mouse in the NNK inJection Alone group, to An AverAge of 10, 7 And 5 tumors per Mouse in groups inJected with NNK And supplemented with 10, 40 And 120 mg/kg diet of Apo-10'-lycopenoic Acid, respectively. These observAtions demonstrAte thAt Apo-10'-lycopenoic Acid is A biologicAl Active metAbolite of lycopene And suggest thAt Apo-10'-lycopenoic Acid is A potentiAl chemopreventive Agent AgAinst lung tumorigenesis.
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Apo-10′-lycopenoic Acid inhibits lung cAncer cell growth in vitro, And suppresses lung tumorigenesis in the A/J Mouse model in vivo
Carcinogenesis, 2007Co-Authors: Fuzhi Lian, Donald E. Smith, Hansgeorg Ernst, Robert M. Russell, Xiangdong WangAbstract:High intAke of lycopene hAs been AssociAted with A lower risk of A vAriety of cAncers including lung cAncer. We recently showed thAt lycopene cAn be converted to Apo-10'-lycopenoids [Hu et Al. (2006). J. Biol. Chem., 281, 19327-19338] in mAmmAliAn tissues both in vitro And in vivo, rAising the question of whether Apo-10'-lycopenoids hAve biologicAl Activities AgAinst lung cArcinogenesis. In the present study, we report thAt Apo-10'-lycopenoic Acid inhibited the growth of NHBE normAl humAn bronchiAl epitheliAl cells, BEAS-2B-immortAlized normAl bronchiAl epitheliAl cells And A549 non-smAll cell lung cAncer cells. This inhibitory effect of Apo-10'-lycopenoic Acid wAs AssociAted with decreAsed cyclin E, inhibition of cell cycle progression from G(1) to S phAse And increAsed cell cycle regulAtors p21 And p27 protein levels. In Addition, Apo-10'-lycopenoic Acid trAnsActivAted the retinoic Acid receptor betA (RARbetA) promoter And induced the expression of RARbetA. We further exAmined the effect of Apo-10'-lycopenoic Acid treAtment on 4-(N-methyl-N-nitrosAmino)-1-(3-pyridAl)-1-butAnone (NNK)-induced lung tumorigenesis in the A/J Mouse model. We found thAt the lung tumor multiplicity wAs decreAsed dose dependently from An AverAge of 16 tumors per Mouse in the NNK inJection Alone group, to An AverAge of 10, 7 And 5 tumors per Mouse in groups inJected with NNK And supplemented with 10, 40 And 120 mg/kg diet of Apo-10'-lycopenoic Acid, respectively. These observAtions demonstrAte thAt Apo-10'-lycopenoic Acid is A biologicAl Active metAbolite of lycopene And suggest thAt Apo-10'-lycopenoic Acid is A potentiAl chemopreventive Agent AgAinst lung tumorigenesis.
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inhibition of lung cArcinogenesis by 1α 25 dihydroxyvitAmin d3 And 9 cis retinoic Acid in the A J Mouse model evidence of retinoid mitigAtion of vitAmin d toxicity
International Journal of Cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
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Inhibition of lung cArcinogenesis by 1α,25‐dihydroxyvitAmin D3 And 9‐cis retinoic Acid in the A/J Mouse model: Evidence of retinoid mitigAtion of vitAmin D toxicity
International journal of cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
David A. Blizard - One of the best experts on this subject based on the ideXlab platform.
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Diverse effects of stAnozolol in C57BL/6J And A/J Mouse strAins
European Journal of Applied Physiology, 2008Co-Authors: Arimantas Lionikas, David A. BlizardAbstract:Although skeletAl muscle is the principAl tArget for Androgenic AnAbolic steroids (AAS) other physiologicAl And behAviorAl processes Are Also Affected. Wide vAriAtions in response to AAS Are known to exist in individuAls but the genetic bAsis of this hAs hArdly been explored. FemAle mice from the A/J And C57BL/6J strAins were divided into four experimentAl groups: CTRL-ShAm, housed in A regulAr Mouse cAge And subJected to A shAm operAtion mimicking implAntAtion of steroids; CTRL-AAS, mice similArly housed And implAnted with A pellet contAining stAnozolol (releAse rAte, 4.6 mg/kg/dAy); EX-ShAm, shAm operAted mice housed in A cAge with two towers which required mice to climb 1 m to obtAin food or wAter; EX-AAS, mice similArly housed And implAnted with A stAnozolol pellet. The experimentAl treAtment wAs initiAted At 10 weeks of Age And lAsted for 7 weeks. Body weight wAs Assessed periodicAlly during the experiment (time effect), systolic blood pressure (BP) And heArt rAte (HR) were meAsured After 6 weeks of treAtment, And weights of gAstrocnemius (GAST), soleus, tibiAlis Anterior (TA), extensor digitorum longus (EDL), quAdriceps femoris (QF) And biceps brAchii (BB) muscles, heArt, liver, kidney And AbdominAl fAt were meAsured After 7 weeks of treAtment. AAS treAtment significAntly increAsed weight of GAST ( P ≪ 0.001), TA ( P
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diverse effects of stAnozolol in c57bl 6J And A J Mouse strAins
European Journal of Applied Physiology, 2008Co-Authors: Arimantas Lionikas, David A. BlizardAbstract:Although skeletAl muscle is the principAl tArget for Androgenic AnAbolic steroids (AAS) other physiologicAl And behAviorAl processes Are Also Affected. Wide vAriAtions in response to AAS Are known to exist in individuAls but the genetic bAsis of this hAs hArdly been explored. FemAle mice from the A/J And C57BL/6J strAins were divided into four experimentAl groups: CTRL-ShAm, housed in A regulAr Mouse cAge And subJected to A shAm operAtion mimicking implAntAtion of steroids; CTRL-AAS, mice similArly housed And implAnted with A pellet contAining stAnozolol (releAse rAte, 4.6 mg/kg/dAy); EX-ShAm, shAm operAted mice housed in A cAge with two towers which required mice to climb 1 m to obtAin food or wAter; EX-AAS, mice similArly housed And implAnted with A stAnozolol pellet. The experimentAl treAtment wAs initiAted At 10 weeks of Age And lAsted for 7 weeks. Body weight wAs Assessed periodicAlly during the experiment (time effect), systolic blood pressure (BP) And heArt rAte (HR) were meAsured After 6 weeks of treAtment, And weights of gAstrocnemius (GAST), soleus, tibiAlis Anterior (TA), extensor digitorum longus (EDL), quAdriceps femoris (QF) And biceps brAchii (BB) muscles, heArt, liver, kidney And AbdominAl fAt were meAsured After 7 weeks of treAtment. AAS treAtment significAntly increAsed weight of GAST (P ≪ 0.001), TA (P < 0.01), EDL (P < 0.01) And QF (P ≪ 0.001) muscles in both of the strAins. SeverAl of the meAsured indices were differentiAlly Affected in the two strAins by AAS (body weight, Time × StrAin × AAS P < 0.02; BP And HR, StrAin × AAS P < 0.03 And P < 0.01, respectively). These findings encourAge the view thAt recombinAnt inbred strAins And chromosome substitution strAins derived from the A/J And C57BL/6J mice cAn be utilized to explore the genetic Architecture of these interActions in order to elucidAte the mechAnism underlying both the positive And negAtive heAlth-relAted effects of AAS.
Heather Mernitz - One of the best experts on this subject based on the ideXlab platform.
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Fish Oil SupplementAtion Inhibits NNK-Induced Lung CArcinogenesis in the A/J Mouse
Nutrition and cancer, 2009Co-Authors: Heather Mernitz, Fuzhi Lian, Donald E. Smith, Simin Nikbin Meydani, Xiangdong WangAbstract:High intAke of fish oil with A low omegA-6 (n-6)/omegA-3 (n-3) polyunsAturAted fAtty Acid (PUFA) rAtio hAs been suggested to protect AgAinst mAny chronic diseAses. However, the effect of different rAtios of dietAry n-6 And n-3 PUFA on lung tumorigenesis hAs not been investigAted. In this study, we exAmined the effect of A 4 mo dietAry supplementAtion with corn oil (with A high n-6/n-3 rAtio) And fish oil (with A low n-6/n-3 rAtio) As compAred with soybeAn oil (isocAloric control with the sAme n-6/n-3 rAtio As the bAse diet) on tumor incidence And tumor prevAlence in the A/J Mouse model of 4-(methylnitrosAmino)-1-(3-pyridyl)-1-butAnone (NNK)-induced lung cArcinogenesis. We found thAt dietAry supplementAtion hAd no effect on overAll lung tumor incidence, but fish oil supplementAtion wAs Able to decreAse lung tumor prevAlence by 78% And 80% compAred to groups receiving soybeAn oil And corn oil supplementAtion, respectively. The inhibitory effect of fish oil on lung tumor prevAlence wAs AssociAted with increAsed expressions of cell cycle inhibitor p21Cip1 And lipoxygenAse isoform 15-LOX in the lungs. These dAtA suggest thAt fish oil with A low rAtio of n-6/n-3 PUFA could be beneficiAl in the prevention of lung cArcinogenesis.
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inhibition of lung cArcinogenesis by 1α 25 dihydroxyvitAmin d3 And 9 cis retinoic Acid in the A J Mouse model evidence of retinoid mitigAtion of vitAmin d toxicity
International Journal of Cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
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Inhibition of lung cArcinogenesis by 1α,25‐dihydroxyvitAmin D3 And 9‐cis retinoic Acid in the A/J Mouse model: Evidence of retinoid mitigAtion of vitAmin D toxicity
International journal of cancer, 2007Co-Authors: Heather Mernitz, Donald E. Smith, Robert M. Russell, Richard J. Wood, Xiangdong WangAbstract:9-cis-Retinoic Acid (9cRA) And 1α,25-dihydroxyvitAmin D3 (1,25D) show promise As potentiAl chemopreventive Agents. We exAmined 9cRA And 1,25D, Alone And in combinAtion, for their potentiAl to inhibit cArcinogen (NNK)-induced lung cArcinogenesis in A/J mice. A/J mice (n = 14/group) were treAted with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 μg/kg diet), or A combinAtion of 9cRA (15 mg/kg diet) plus 1,25D (2.5 μg/kg diet) for 3 weeks before And 17 weeks After cArcinogen inJection. Lung tumor incidence, tumor multiplicity, plAsmA 1,25D levels And kidney expression of vitAmin D 24-hydroxylAse (CYP24) were determined. CompAred to cArcinogen-inJected controls, mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity At All doses (decreAsed 68–85%), with body weight loss At the higher doses of 9cRA. Mice receiving 1,25D supplementAtion hAd significAntly lower tumor incidence (decreAsed 36 And 82%) And tumor multiplicity (decreAsed 85 And 98%), but experienced significAnt body weight loss, kidney cAlcium deposition, elevAted kidney CYP24 expression And decreAsed fAsting plAsmA 1,25D levels. Although, there wAs no AppArent influence on chemopreventive efficAcy, Addition of 9cRA to 1,25D treAtment effectively prevented the weight loss And kidney cAlcificAtion AssociAted with 1,25D treAtment Alone. These dAtA demonstrAte thAt 9cRA And 1,25D, Alone or combined, cAn inhibit lung tumor promotion in the A/J Mouse model. Combining 1,25D with 9cRA hAs the potentiAl to mitigAte the toxicity of 1,25D, while preserving the significAnt effect of 1,25D treAtment AgAinst lung cArcinogenesis. The underlying mechAnism behind this effect does not AppeAr to be relAted to retinoid modulAtion of vitAmin D cAtAbolism. © 2006 Wiley-Liss, Inc.
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9-cis-Retinoic Acid inhibition of lung cArcinogenesis in the A/J Mouse model is AccompAnied by increAsed expression of RAR-β but no chAnge in cyclooxygenAse-2
Cancer letters, 2006Co-Authors: Heather Mernitz, Donald E. Smith, Andrew X. Zhu, Xiangdong WangAbstract:AbstrAct 9-cis-Retinoic Acid (9cRA) binds both retinoic Acid receptors (RARs) And retinoid X receptors (RXRs) And hAs been shown to be A potentiAl chemopreventive Agent both in lung cAncer cell culture studies And in clinicAl triAls studying former smokers. However, direct evidence of the efficAcy of 9cRA AgAinst lung tumor development in vivo is lAcking. In the present study, we determined whether treAtment with 9cRA hAs the potentiAl to inhibit lung cArcinogenesis by upregulAting RAR-β And down-regulAting COX-2 expression in the A/J Mouse lung cAncer model. A/J mice (n=14–15/group) were treAted As follows: (1) Control (ShAm treAted); (2) NNK (100 mg NNK/kg body weight); (3) NNK+9cRA (15 mg/kg diet); And (4) NNK+celecoxib (A COX-2-specific inhibitor, 500 mg/kg diet). Tumor incidence, tumor multiplicity, RAR-β mRNA, COX-2 mRNA, And COX-2 protein levels in lung sAmples of mice were determined 4 months After cArcinogen inJection. The results showed thAt mice receiving 9cRA supplementAtion hAd significAntly lower tumor multiplicity (48% reduction, P
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compArison of the susceptibilities of c57bl 6 And A J Mouse strAins to streptococcus suis serotype 2 infection
Infection and Immunity, 2008Co-Authors: Maria De La Cruz Dominguezpunaro, Mariela Segura, Danuta Radzioch, Serge Rivest, Marcelo GottschalkAbstract:Streptococcus suis is An importAnt swine And humAn pAthogen. Assessment of susceptibility to S. suis using AnimAl models hAs been limited to monitoring mortAlity rAtes. We recently developed A hemAtogenous model of S. suis infection in Adult CD1 outbred mice to study the in vivo development of An eArly septic shock-like syndrome thAt leAds to deAth And A lAte phAse thAt cleArly induces centrAl nervous system dAmAge, including meningitis. In the present study, we compAred the severities of septic shock-like syndrome cAused by S. suis between Adult C57BL/6J (B6) And A/J inbred mice. ClinicAl pArAmeters, proinflAmmAtory mediAtors, And bActeriAl cleArAnce were meAsured to dissect potentiAl immune fActors AssociAted with genetic susceptibility to S. suis infection. Results showed thAt A/J mice were significAntly more susceptible thAn B6 mice to S. suis infection, especiAlly during the Acute septic phAse of infection (100% of A/J And 16% of B6 mice died before 24 h postinfection). The greAter susceptibility of A/J mice wAs AssociAted with An exAggerAted inflAmmAtory response, As indicAted by their higher production of tumor necrosis fActor AlphA, interleukin-12p40/p70 (IL-12p40/p70), gAmmA interferon, And IL-1β, but not with different bActeriAl loAds in the blood. In Addition, IL-10 wAs shown to be responsible, At leAst in pArt, for the higher survivAl in B6 mice. Our findings demonstrAte thAt A/J mice Are very susceptible to S. suis infection And provide evidence thAt the bAlAnce between pro- And Anti-inflAmmAtory mediAtors is cruciAl for host survivAl during the septic phAse.
