Nad Quinone Oxidoreductase One Gene Nad Dehydrogenase Family Biology Essay

The enzyme serves as a quinone reductase in connexion with the junction reactions of hydroquinones involved in the detoxification pathways every bit good as in the biosynthetic procedures such as vitamin K-dependent gamma-carboxylation of glutamate residues in the synthesis of the factor II. [ 9 ] .

It besides involved in the azotic oxide biogenesis, response to toxin, synaptic transmittal, cholinergic, xenobiotic metamorphosis. [ 10 ] . A broad assortment of substrates such as quinones reduces two negatrons which are catalyzed by NQO1. The DT-diaphorase enzyme reduces the quinone-imines, azo and nitro compounds but the most efficient substrate is quinone. The enzyme maps through the hydride transportation mechanism and requires a pyridine nucleotide cofactor.

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Both the NADPH and NADH returns with the decrease of negatrons in the same form. After the onslaught of the free group, it can bring forth antioxidant signifiers of both ubiquinone and vitamin E. The capableness to protect the cells from oxidative challenge and the ability to diminish the quinones through an obligate two negatron mechanism that precludes coevals of reactive O groups and considered that NQO1 is an enzyme of chemoprotective.

NQO1 stabilizes tumour suppresser cistron p53.Its interaction with the p53 in protein-protein interaction has been shown. Certain compounds such as antitumor quinones are bioactivated by the two negatron decrease.So NQO1 serves like an triping enzyme [ 11 ] .

Why NQO1 enzyme is described as an anticancer agent?

NQO1enzyme is described as anticancer agent because formation of B [ a ] P DNA adduct which is generated by CYP450 reductase reduced by NQO1enzyme. [ 39 ] .

Quinone metamorphosis tract

The two negatron decrease of quinoid compounds into hydroquinone is catalyzed by NQO1 which is a cytosolic spirit enzyme.

Phase-1enzyme such as Cytochrome p450 catalyzes one negatron decrease from quinone. This procedure formed alkylating species and free groups as the metabolite undergo car oxidization under aerophilic status. NQO1 forestalling quinones from come ining the one negatron decrease and two negatron decrease is catalyzed by NQO1 which causes the formation of the less toxic hydroquinones that are excreted readily when conjugated.

In this manner cell protection from oxidative harm occurs by NQO1 [ 39 ] .

4. Signing

The AhR represser and the stage II xenobiotic metabolising enzyme NAD ( P ) H: quinone oxidoreductase ( NQO1 ) are induced by polyaromatic hydrocarbons. It is believed that the AhR and AhR repressor represent a xenobiotic signal transduction negative feedback cringle. AhR represser written text induced by the liganded AhR that expressed the AhR represser. It besides inhibits the AhR map. [ 22 ] .

Recent surveies suggest that the AhR besides plays a function in tumour patterned advance, i.e. from a benign to a malignant tumour, in carnal theoretical accounts and really likely besides in worlds, beside its map in tumour induction and publicity. There was found that AhR non merely play a function in PAH-dependent tumour induction but besides it is involved in the PAH-dependent tumour publicity and patterned advance. It was presently indicated that the AhR induces cistron written text beyond metamorphosis. In several cell lines, the activation of the AhR leads to cell rhythm apprehension in G1-phase, which is due to a direct association of the hypophosphorylated retinoblastoma protein ( pRB ) with the AhR. Thus patterned advance into S-phase is inhibited. ( 36 ) .

The written text factor, atomic factor kappa B modulates AhR signaling was found. For cellular proliferation, distinction and motility, cell-cell contact is known to be a critical regulator. Proliferation suppression by cell-cell contact is by and large referred to as contact suppression.It is besides known as contact-dependent suppression of growing. Contact suppression is thought to be continuously active, playing a critical function in the repression of bodily cell proliferation in grownup tissues. When contact suppression is released, it was found that cell is proliferated abnormally. Either due to increased proliferation or decreased degree of programmed cell death, tumour publicity is characterized by imbalanced proliferation. It is likely that contact suppression loss is a possible event during publicity of the tumour.

[ 23 ] .

PAH

Fig-2-AhR signaling tract

The Aryl hydrocarbon Receptor ( AhR ) is a written text factor. It is activated through a ligand.

It was originally discovered because of its stimulation by a assortment of the aromatic hydrocarbons with the benzo [ a ] pyrene as paradigm. The AhR is activated by the PAH. Here, PAH is acted as a ligand. The above fig shows that the unliganded receptor AhR forms a complex with two heat daze protein90 ( Hsp90 ) molecules, XAP2 and co-chaperones p23 in the cytosol.

Whenever PAH ( ligand ) binds to the AhR, the look of the cistron is induced. The ligand adhering consequences in AhR atomic translocation, the chaperone proteins dissociation, heterodimerization with ARNTand subsequent binding of the AhR-ARNT heterodimer to dioxin-responsive elements ( DREs ) with the consensus nucleus acknowledgment sequence 5′-TNGCGTG-3 ‘ . 5’-TNGCGTG-3 ‘ is besides known as xenobiotic-responsive elements ( XREs ) . Several cistrons encoding stage I and II xenobiotic metabolizing enzymes, such as NQO1 leads to transactivation. AhR pathway activation occur by PAHs that ‘s why leads to their detoxication and elimination and at the same clip, to their metabolic activation to genotoxic compounds. [ 23 ]

5.

Mechanism

5.1- Carcinogen designation

The baccy fume carcinogens impacting the NQO1gene are benzo [ a ] pyrene which is a PAH, responsible for vesica malignant neoplastic disease [ 13 ] [ 39 ] , PAHs for esophageal malignant neoplastic disease [ 14 ] and benzine for leukaemia [ 15 ] .

5.2-Interaction mechanism

Bladder

What is bladder?

Bladder is a muscular, balloon like organ that collects the piss from each kidney to bladder through a narrow tubing, ureter. The piss from vesica is eliminated through another narrow tubing called urethra [ 44 ] .

Interaction mechanism between vesica and carcinogen ( B [ a ] P )

Tumor in the vesica develops due to its interactions with the carcinogenic substances like polyaromatic hydrocarbons ( PAH ) in the baccy smoke instead than a direct exposure to them. PAH targets the vesica through blood [ 16 ] .

The carcinogens from the baccy fume are directed from lungs into the blood watercourse and make all parts of the organic structure. The blood is filtered by kidneys and concentrated into the piss. The piss is stored and discharged from the vesica, therefore the carcinogens in the piss saddle horse up and targets the liners of the vesica walls made up of the urothelial cells. This harm to the cell liner makes the tobacco user more likely to develop vesica malignant neoplastic disease [ 17, 18 ] .

Familial polymorphisms of enzymes that catalyze the exogenic or the endogenous carcinogens may find the single susceptibleness to development of malignant neoplastic disease. Most of the chemical carcinogens in coffin nails require metabolic activation by stage I enzymes and detoxification by stage II enzymes such as NAD ( P ) H: quinone oxidoreductase 1 ( NQO1 ) . Metabolic activation of the PAHs by stage I enzymes lead to oxidised merchandises, including quinones, ensuing in the reactive O species ( ROS ) . In contrast, detoxification of certain carcinogens lead to the less-toxic and more hydrophilic derived functions, which are readily excreted. NQO1, an indispensable two-electron reductase and protect the cells from oxidative harm by diminishing ROS and cut downing formation of DNA adducts by benzo [ a ] pyrene 3, 6-quinone, one of the carcinogen identified in the coffin nail fume. However, NQO1 can besides catalyse the activation of some procarcinogens found in coffin nail fume. The activity of the NQO1 enzyme depends on the polymorphisms at the NQO1 venue.

The major polymorphism of the NQO1 involves a individual base C to T passage at nucleotide 609 ( codon 187 ) of exon 6, which codes for a proline ( Pro ) to serine ( Ser ) amino acerb permutation in protein. Lack of the protein as a consequence of NQO1 T/T genotype is associated with the accelerated debasement of the mutant NQO1 protein. Therefore, the discrepancy allelomorph ( T ) of NQO1 is associated with decreased enzymatic activity, and may take to diverse abilities of the metabolic activation and detoxification.

Cigarette smoke is thought to be a major hazard factor for the vesica malignant neoplastic disease, and smoke contains many carcinogens including the benzo [ a ] pyrene. NQO1 can change over benzo [ a ] pyrene intermediates to the less-toxic metabolites. The NQO1 discrepancy genotypes that result in the decreased enzyme activity may take to development of the malignant neoplastic disease [ 19 ] .

B [ a ] P metamorphosis

Fig-3-Interaction mechanism between phase-1enzyme cytochrome p450s and phase-2 enzyme NQO1in the metamorphosis of B [ a ] P [ 38 ] .Multiple reactions are catalyzed by phase-1enzyme such as CYP450. The enzyme drama a major function in the activation of carcinogen such as B [ a ] P which is a PAH.

Phase-2 enzymes catalyze junction of the reactive intermediates and ensuing urine formation through the procedure of the elimination. It was found that higher degrees of reactive carcinogen metabolites are produced due to higher activation of carcinogen by phase-1 enzyme and lower detoxification by phase-II enzymes. Then higher degree of reactive carcinogen metabolites bind to the Deoxyribonucleic acid. After that binding, DNA adducts are formed. If the DNA fix enzymes are unable to take the adducts, it replicate mistakes that initiate the carcinogenic casecade and causes mutant [ 38 ] .

It was found that oxidative metabolite of benzo ( a ) pyrene [ benzo ( a ) pyrene 3, 6-quinones ] causes mutant in NQO1which is present in baccy fume [ 39 ] .

Chemistry

Fig-4-chemical construction of benzo [ a ] pyrene [ 42 ]Fig-5- Benzo [ a ] pyrene metamorphosis demoing DNA harm [ 40 ] , [ 41 ] .Quinones green goodss ROS by redox rhythm between quinone and diphenol. B [ a ] Pis eliminated by elimination of glutathione and glucorunides conjugates. Theprimary measure for B [ a ] P riddance is oxidation by CYP1A1 and CYP1B1.

B [ a ] P oxidization by CYP1A1and CYP1B1 is besides responsible for the bioactivation of the carcinogenic metabolites. For the detoxification of the primary metabolites, junction with glutathione and glucorunic acid are indispensable. B [ a ] P-3, 6-quinones signifiers B [ a ] P diphenoles and the reaction is catalyzed by NQO1 enzyme. Then it prevents the formation of semiquinones and redox rhythm. Later it generates ROS [ 41 ] .

Relation of benzine with vesica malignant neoplastic disease

In chromosome 16q22, the NQO1 cistron is located.

In this cistron many SNPs have been discovered.At nucleotide place 609, a nonsynonymous SNP was found.At codon 187 in the protein ( dbSNP ID: rs1800566 ) , the discrepancy is a C-to-T passage and consequences in a proline to serine amino acerb permutation. Harmonizing to the in vitro surveies, the variant allelomorph consequences in decreased enzymatic activity. It was found that C-T passage at codon 187results pro-ser permutation associated with benzene toxicity [ 39 ] .

Change

NQO1 enzyme depends on the polymorphisms at the NQO1 venue.

The major polymorphism of the NQO1 involves a individual base C to T passage at nucleotide 609 ( codon 187 ) of exon 6, which codes for a proline ( Pro ) to serine ( Ser ) amino acerb permutation in protein. Lack of the protein as a consequence of NQO1 T/T genotype is associated with the accelerated debasement of the mutant NQO1 protein. Therefore, the discrepancy allelomorph ( T ) of NQO1 is associated with decreased enzymatic activity, and may take to diverse abilities of the metabolic activation and detoxification.

Cigarette smoke is thought to be a major hazard factor for the vesica malignant neoplastic disease, and smoke contains many carcinogens including the benzo [ a ] pyrene. NQO1 can change over benzo [ a ] pyrene intermediates to the less-toxic metabolites. The NQO1 discrepancy genotypes that result in the decreased enzyme activity may take to development of the malignant neoplastic disease [ 19 ] .

Esophagus

What is oesophagus?

Oesophagus is otherwise known as nutrient pipe. It is a hollow tubing which carries liquids and nutrients from the pharynx to the tummy [ 45 ] .

How smoking causes DNA harm in oesophageal malignant neoplastic disease?

Genomic changes

Chromosomal instability

Cancer

Cellular proliferation

Telomere shortening

Deoxyribonucleic acid harm

Oesophageal tissue

Inflammation

Systemic redness

Cigarette

Smoking

Fig-6-Inflammation and oesophageal adeno carcinomaIt was found that Cigarette smoking causes redness systemically and in the oesophageal epithelial tissue by get downing smoke merchandises. A chronic province of systemic and localised redness and oxidative emphasis promotes the DNAdamage, cell proliferation and telomere shortening that addition the hazard of developing ringers incorporating the small-scale and large-scale genomic changes, finally taking to widespread chromosomal instability and oesophageal glandular cancer. [ 21 ]

How the carcinogens affect the map of the Deoxyribonucleic acid in gorge?

Familial polymorphisms of enzymes that catalyze the exogenic or the endogenous carcinogens may find the single susceptibleness to development of malignant neoplastic disease.

Most of the chemical carcinogens in coffin nails require metabolic activation by stage I enzymes and detoxification by stage II enzymes such as NAD ( P ) H: quinone oxidoreductase 1 ( NQO1 ) . Metabolic activation of the PAHs by stage I enzymes lead to oxidised merchandises, including quinones, ensuing in the reactive O species ( ROS ) . In contrast, detoxification of certain carcinogens lead to the less-toxic and more hydrophilic derived functions, which are readily excreted. NQO1, an indispensable two-electron reductase and protect the cells from oxidative harm by diminishing ROS and cut downing formation of DNA adducts by benzo [ a ] pyrene 3, 6-quinone, one of the carcinogen identified in the coffin nail fume. However, NQO1 can besides catalyse the activation of some procarcinogens found in coffin nail fume.

Cigarette smoke is thought to be a major hazard factor for the vesica malignant neoplastic disease, and smoke contains many carcinogens including the benzo [ a ] pyrene. NQO1 can change over benzo [ a ] pyrene intermediates to the less-toxic metabolites. The NQO1 discrepancy genotypes that result in the decreased enzyme activity may take to development of the malignant neoplastic disease. [ 19 ] .

Chemistry

Lapp as vesica.

Change

NADP ( H ) : Quinone oxidoreductase 1 ( NQO1 ) is one of the most of import enzyme. Some un­stable PAH metabolites are extremely reactive and may assail the Deoxyribonucleic acid molecule in the procedure of the NQO1 enzyme metabolic reaction. Then PAH DNA adducts are formed. NQO1 detoxify a big no. of man-made and environmental chemicals. In the 609th codon of NQO1DNA, a polymorphism of C-T leads to the formation of the NQO1*2 allelomorph. The NQO1*2 allelomorph is weak in its biochemical activity.

There are merely 2-4 % enzymatic activity found in the NQO1 T allelomorph in comparing to its wild type signifier. NQO1 m-RNA is expressd by the polymorphous NQO1allele ( T/T ) . But the uttered m-RNA has no noticeable protein because the proteosomal system quickly degraded the mutant NQO1 protein. A proline to serine alteration in the 187th amino acerb location of the NQO1 protein sequence caused by C-T permutation. It was found that oxidative compounds such as PAH stimulates the NQO1 cistron expression.There was found a relation between esophageal tissue look and their implicit in NQO1*2 allelomorph ( C609T ) genotypes [ 43 ] .

Leukemia

What is leukemia?

Leukemia is the malignant neoplastic disease of blood and bone marrow because of an unnatural proliferation of blood cells, by and large leukocytes ( WBCs ) [ 24, 25 ]

How coffin nail fume causes DNA harm in blood?

Leukemia-causing chemicals like benzine nowadays in coffin nail fume. [ 27 ] .It is a known human carcinogen.30 % addition hazard of leukaemia acquiring through smoke. 14 % of all grownup leukaemia instances causes through smoke. It is besides regarded as a primary cause of leukaemia. [ 24 ] , [ 25 ] .

It was found and considered that the chief cause of leukaemia is cigarette smoke. This is a major hazard factor besides. Benzene, polonium-210, and polycyclic aromatic hydrocarbons ( PAHs ) , these chemicals are present in baccy fume.

Lungs absorbed these carcinogens.These carcinogens are spread through the blood stream. These carcinogens damage the Deoxyribonucleic acid within blood cells. [ 25 ] . Hence, normal bone marrow cells are transformed to leukemic cells due to DNA harm. [ 26 ] . There are found that some pieces are lost from WBC from their DNA.It was shown that unnatural leukemic cells proliferate over by over through reproduction.

An immature blast is produced that will non maturate decently like normal blood cells. Those leukemic cells will non decease and generation occurred until production of unnatural cells than normal healthy blood cells. Due to translocation, the mutant besides occurs where one portion of chromosome displaces and attached to other portion of the chromosome.

Normal DNA sequences will interrupt due to the translocation. It leads stimulates the growing of the tumour and cause bar of tumour suppression [ 28 ] .One in four instances of acute myelogenous leukaemia ( AML ) is the consequence of coffin nail smoke is estimated. [ 25 ] .Another major beginning of public exposure to benzene is cigarette smoke. Approximately 2 mg/day was inhaled by a pack-a-day tobacco user. In NQO1gene, inherited Polymorphism encodes carcinogen activation and detoxification. It contributed indirectly to leukemia.

The NQO1 enzyme is involved in the metamorphosis of benzine [ 29 ] .MPONQO1CYP2E1CYP2E1ToxicityQuinoneDI AND TRI HYDROXY BENZENE ( HQ, CAT, BT )PhenolBENZENE OXIDEBenzeneFigure-7- benzine metamorphosis pathway taking to toxicity and detoxificationThe diagram above shows that the hepatic enzyme CYP2E1 metabolized benzineBenzene signifiers benzene oxide through metabolisation that instantly forms phenol. Again phenol is metabolized by CYP2E1 which forms di and tri hydroxyl benzine such as catechol ( CAT ) , hydroquinone ( HQ ) , and 1, 2, 4-benzenetriol ( BT ) .

Thus it plays an indispensable function in toxicity of benzine by triping it to toxic metabolites. Hydroquinone is converted to benzoquinone in the bone marrow by Myeloperoxidase.Benzoquinones are regarded as hematotoxin and genotoxin compounds.

[ 30 ] . NQO1 converted benzo quinones back to less toxic carbolic acids. Peoples lack important activity of NQO1 doing them potentially susceptible to benzene toxicity.

A homozygous mutant ( C -T ) at place 609 in the NQO1 cistron is caused by this fluctuation. It was found thatNQ01609 mutant would be susceptible to benzene hematotoxicity with high CYP2E1 activity.NQO1 is besides a hazard factor for leukaemia. Benzene poising hazard increased at a7.6 fold by homozygous NQO1 mutation allelomorph [ 29 ] .

Those who are homozygous for the point mutant, the NQO1 protein and activity are absent in them [ 30 ] .

Chemistry

Fig-8-St of benzene-C6H6 [ 35 ]Benzene is a chemical compound. The chemical expression of benzine is C6H6.Itis a colourless aromatic hydrocarbon which is a known carcinogen [ 46 ] .

Benzene metamorphosis

A critical function in benzene toxicity was played by benzene metamorphosis.

It was besides found that hepatic metamorphosis play a critical function in benzene metamorphosis.Secondary metamorphosis of benzine metabolites contributed to toxicity in the bone marrow [ 36 ] .[ 36 ] Fig-9-Benzene metabolic tract

First step-Phenol formation

CYP450+NADPH+H+ +O2 CYP450+NADPHThe above reaction shows that H2O2 generated by cytochrome p450 when moving as oxidases of NADPH.HOOH 2 *OHThis reaction indicates the coevals of hydroxyl groups.Benzene + * OH phenolIt indicates that hydroxyl groups formed from H2O2 hydroxylated to benzene to organize phenol.

The first merchandise is benzene oxide. Phenol is produced from benzine oxide by nonenzymatically rearrangement.

Second step-formation of benzenedihydrodiol

Epoxide hydrolase hydrated benzene oxide to organize 1, 2-benzene dihydrodiol.

Third step- catechol formation from benzenedihydrodiol

Benzene dihydrodiol signifiers catechol through oxidation.The oxidization is carried out by the enzyme dihydrodiol dehydrogenase.

Fourth step-Formation of hydroquinone or catechol from phenol

The farther hydroxylation of phenol gives rise hydroquinone or catechol [ 36 ] .

Fifth step-Formation of 1, 2, 4-trihydroxy benzine

The other names of 1,2,4-Trihydroxybenzene are Hydroxyhydroquinone ; Benzene-1,2,4-triol, 1,2,4-Benzenetriol [ 37 ] .Either hydroxylation of hydroquinone or catechol produces 1,2,4-trihydroxy benzine [ 36 ] .

Sixth step-Formation of benzo quinone

Hydroquinone is converted to benzo quinone in bone marrow by Myeloperoxidase. Benzo quinones are regarded as hematotoxin and genotoxin compounds.

[ 30 ]NQO1 converted benzo quinones back to less toxic carbolic acids. Peoples lack important activity of NQO1 doing them potentially susceptible to benzene toxicity [ 29 ] .

Potential mechanism for benzine toxicity

Benzene metabolites produced in the liver.

It is so transported to the bone marrow. Benzene damaged the Deoxyribonucleic acid in the bone marrow.DNA harm result the depression of bone marrow which causes aplastic anemia.Then it leads to marrow dysplasia and finally it leads to acute leukaemia.

Fig-Pathway of harm of Deoxyribonucleic acid by benzine in bone marrow cellsThe tract shows two mechanisms.

First mechanism

In first mechanism the tract shows that benzine metabolites cause the harm of the DNA.Benzene metabolic activation bind to the DNA covalently and after adhering mutagenic events are produced that are expressed as leukaemia.

Second mechanism

In 2nd mechanism the tract shows that metabolite production which causes oxidative emphasis. Through oxidative emphasis oxidative harm to DNA occurred [ 36 ] .

Oxidative emphasis and benzine toxicity

Oxidative emphasis caused by benzine toxicity through benzine metabolites. Hydroquinones are oxidized to organize p-benzo quinone.p-benzoquinone bind covalently to the cellular supermolecules or glutathione. It is extremely reactive. Benzene metabolites are involved in the oxidation-reduction cycling.

Benzene metabolites take part in car oxidization of a decreased signifier of the metabolite.Thus reactive O and an oxidised species are produced from benzine metabolites. Bone marrow is one of the richly oxygenated organ.

It has the ability to bring forth reactive O species. From the benzine metabolites four negatrons reduced from O and generate H peroxide, hydroxyl extremist and superoxide anion groups. The starting stuffs are produced through the oxidized metabolite by undergoing their decrease of spirit protein. Then the get downing stuff reenters the redox rhythm. It was found that hydroquinone-p-benzo quinone reenter oxidation-reduction rhythm.Fig-10-benzo quinone decrease by FPH2 reductaseThe figure shows that p-benzo quinone decrease returns through CYP450 reductase.Step-1Semiquinone anion group is the first merchandise.

Step-2ASemiquinone is reduced once more by FPH2.Step-2BIn this measure protonation occurs. In the 2nd decrease hydroquinone is formed.

The following measure in oxidation-reduction cycling is reoxidation to p-benzo quinone would be inhibited because hydroquinone and is the substrate for car oxidization taking to the formation of superoxide anion. Therefore at physiological pH it is improbable that hydroquinone-p-benzo quinone undergoes redox cycling.Fig-11-Interaction of p-benzo quinone with glutathione ( slow car oxidization )If p-benzo quinone is non reduced. It reacts with GSH and premercapturic acid of hydroquinone is produced from this reaction, which once more produces mercapturic acid, and taking to the production of reactive O species through slow car oxidization.

Fig- 14-The formation of p-benzo quinone 2,3-oxide from p-benzo quinone and its metabolic destiny

Step-1

By the add-on of the HOOH, p-Benzo quinone is converted to its epoxides.Step-2Either by one-electron decrease ( 1 ) catalyzed by P450 reductase or by two-electron decrease ( 2 ) catalyzed by DT diaphorase, p-Benzoquinone is reduced to 1,2,4-benzenetriol.Step-3Chemical reaction of GSH with p-benzo quinone 2, 3-oxide leads to the formation of glutathionyl 1, 2, 4-benzenetriol [ 36 ] .

Change

Due to a C-T permutation at nucleotide 609 in the complementary DNA, a polymorphism exist which giving rise to a missense mutant in codon 187 ( proline-serine ) . The frequence of an demobilizing polymorphism in NQO1 appears to be increased in myeloid leukaemia patients with abnormalcies of chromosomes 5 and/or 7 but non in those with balanced translocations. Thus wholly lack enzyme activitySusceptible to leukemogenic alterations induced by carcinogens in persons who are homozygous for the demobilizing allelomorph of NQO1 [ 30, 31 ] .

It was besides found that decreased enzyme activity associated with persons with the NQO1*2 discrepancy [ 32 ] . It was observed that statistically important association was found between NQO1 C609T polymorphism and hazard of chronic myelocytic leukaemia [ 33 ] .It wasSuggested that NQO1C609T polymorphism caused leukaemia in childrens. So NQO1 C609T polymorphism is a major hazard factor for childhood leukaemia. [ 34 ] .

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