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Resveratrol is known to imitate energy restriction in high-fat diet fed rat and mice. RES effectively combated gain in body weight, decreased intra - abdominal fat, and dropped serum triglycerides, cholesterol, and free fatty acids FFA levels in obese Zucker fatty rats [ 3 ]. Little is known regarding the safety of RES in control rats and hardly any evidence exists concerning its effect on body weight.

Recently, it was found that there is no adjuvant effect of RES on energy restriction for obesity treatment [ 4 ]. In accordance with the study of Majumdar et al. At present there are many therapeutic agents that decrease body weight but they have contrary side effects, not many therapeutic agents are known that decrease body weight without causing severe side effects. Though there has been a great deal of studies on the protective effects of resveratrol on obesity using rat as a model but there were reports on its effects on body weight especially in the control rats.

We found that when resveratrol was given to control rats and OVX rats there was a reduction in their gain of body weight in comparison to their respective untreated groups.

We want to address here that why resveratrol acts in a differential manner in the control and OVX menopausal model rats. Standard soya free, isonitrogenous and isocaloric diet was made available ad libitum with free access to drinking water.

Rats were handled and euthanized in full agreement with the institutional guidelines for the care and management of laboratory animals. Animals in the resveratrol treatment groups were first given resveratrol containing pellets after calculating the required weight of the pellets based on the individual animal body weight and once they have been finished, the diet tray was replenished with diet without resveratrol. Dose preparation and administration were made in dark to evade isomerization of trans-resveratrol to the cis form.

After the treatment period, the rats were kept for fasting overnight and were sacrificed. Blood was withdrawn by cardiac puncture for estimation of serum parameters. The success of anesthesia was evaluated by failure of the wink reflex and by the lack of reaction to pinching of the foot. Using aseptic conditions, a skin incision was made at the dorsal midline slightly caudal to the last rib followed by a flank incision of the abdominal muscles. The ovary was exteriorized. The proximal end of the uterine horn was then ligated with absorbable sutures 4—0 chronic gut , incised and removed with the attached ovary.

05 Ebong Himu By Humayun Ahmed [1995] [Nirjoy].pdf

The second ovary was removed from the opposite side in the same manner. Using absorbable sutures, the abdominal muscle incision was closed. Furthermore, more thorough characterization of the roles of the different DNA repair mechanisms in the various brain cell types, such as neurons, astrocytes, oligodendrocytes, microglia and Schwann cells, is another key focus going forward.

How this information can ultimately be used in designing strategic clinical interventions is a major challenge ahead. While mitochondria maintain their own genome, most mitochondrial proteins are encoded by the nuclear genome.

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Nevertheless, maintaining mitochondrial DNA integrity is critical for preserving mitochondrial function. As such, it is becoming more and more evident that several DNA repair proteins that operate within the nucleus, also function within mitochondria, often being translocated to this organelle as a distinct protein isoform.

Indeed, several of the human disorders described above are now recognized as having mitochondrial dysfunction as part of the clinical disease. For example, the CS proteins [71,72,,], TDP1 [], Aprataxin [] and PNKP [,], have all been recently shown to reside in the mitochondria and contribute to maintaining proper mitochondrial function.

Determining the relative contribution of their role s in the nucleus versus the mitochondria in terms of the disease etiology, particularly the associated neuropathology, is a critical undertaking going forward. Iyama and Wilson Page 18 discussion of mitochondrial DNA repair, the reader is directed to several comprehensive reviews [,,]. Peter Sykora and Magdalena Misiak for their critical reading of the manuscript.

Reference List 1. Lindahl T. Instability and decay of the primary structure of DNA. Hoeijmakers JH. DNA damage, aging, and cancer. N Engl J Med. DNA repair deficiency in neurodegeneration. Prog Neurobiol. The involvement of DNA-damage and -repair defects in neurological dysfunction. Am J Hum Genet. Defective DNA repair and neurodegenerative disease. The mechanics of base excision repair, and its relationship to aging and disease. McKinnon PJ. DNA repair deficiency and neurological disease.

Nat Rev Neurosci. Premature aging and cancer in nucleotide excision repair- disorders. Caldecott KW. Single-strand break repair and genetic disease. Nat Rev Genet. Loveless A. Possible relevance of O-6 alkylation of deoxyguanosine to the mutagenicity and carcinogenicity of nitrosamines and nitrosamides. Detection of O6-methylguanine, O4-methylthymine and O4-ethylthymine in human liver and peripheral blood leukocyte DNA.

A highly sensitive and specific method for quantitation of O-alkylated DNA adducts and its application to the analysis of human tissue DNA. Environ Health Perspect. Xiao W, Samson L. In vivo evidence for endogenous DNA alkylation damage as a source of spontaneous mutation in eukaryotic cells. Expression of the endogenous O6- methylguanine-DNA-methyltransferase protects Chinese hamster ovary cells from spontaneous G: T transitions.

Cancer Res. O6-methylguanine in DNA inhibits replication in vitro by human cell extracts. O6-methylguanine-induced replication blocks. J Mol Biol. Roles of transcription and repair in alkylation mutagenesis. Mutat Res. Iyama and Wilson Page 19 Nucleic Acids Res.

O6-methylguanine induces altered proteins at the level of transcription in human cells. Jiricny J.

The multifaceted mismatch-repair system. Nat Rev Mol Cell Biol. Modrich P. Mechanisms in eukaryotic mismatch repair.

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J Biol Chem. Ubiquitination-dependent proteolysis of O6-methylguanine-DNA methyltransferase in human and murine tumor cells following inactivation with O6-benzylguanine or 1,3-bis 2-chloroethyl nitrosourea. Implication of localization of human DNA repair enzyme O6-methylguanine-DNA methyltransferase at active transcription sites in transcription-repair coupling of the mutagenic O6-methylguanine lesion.

Mol Cell Biol. Enzyme activity, promoter methylation and immunohistochemistry. Biochim Biophys Acta. Goth R, Rajewsky MF. Persistence of O6-ethylguanine in rat-brain DNA: Kleihues P, Bucheler J. Long-term persistence of O6-methylguanine in rat brain DNA. Mechanism of perinatal tumor induction by neuro-oncogenic alkylnitrosoureas and dialkylaryltriazenes. Natl Cancer Inst Monogr. O6-Alkylguanine-DNA alkyltransferase content in synchronised human cancer cells.

Cancer Chemother Pharmacol. Promoter structure and cell cycle dependent expression of the human methylpurine-DNA glycosylase gene. Targeted disruption of the DNA repair methyltransferase gene renders mice hypersensitive to alkylating agent. Methylnitrosourea- induced tumorigenesis in MGMT gene knockout mice. The prevention of thymic lymphomas in transgenic mice by human O6-alkylguanine-DNA alkyltransferase.

Rapid repair of O6-methylguanine-DNA adducts protects transgenic mice from N-methylnitrosourea-induced thymic lymphomas. Iyama and Wilson Page 20 O6-methylguanine- DNA methyltransferase protects against nitrosamine-induced hepatocarcinogenesis. Roos WP, Kaina B. DNA damage-induced apoptosis: Cancer Lett. DNA repair modulates the vulnerability of the developing brain to alkylating agents. Molecular mechanisms of mammalian global genome nucleotide excision repair.

Chem Rev. Regulation of endonuclease activity in human nucleotide excision repair. Xeroderma pigmentosum, trichothiodystrophy and Cockayne syndrome: Recognition of DNA damage by the Rad4 nucleotide excision repair protein.

An aromatic sensor with aversion to damaged strands confers versatility to DNA repair. PLoS Biol. Scharer OD. Achieving broad substrate specificity in damage recognition by binding accessible nondamaged DNA. Mol Cell. Strand- and site-specific DNA lesion demarcation by the xeroderma pigmentosum group D helicase.

Two-step recognition of DNA damage for mammalian nucleotide excision repair: Recognition of helical kinks by xeroderma pigmentosum group A protein triggers DNA excision repair. Nat Struct Mol Biol. EMBO J. Mechanism of open complex and dual incision formation by human nucleotide excision repair factors. Sequential recruitment of the repair factors during NER: Iyama and Wilson Page 21 Nucleotide excision repair of DNA with recombinant human proteins: Genes Dev.

Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo. Selby CP, Sancar A. Cockayne syndrome B protein regulates the transcriptional program after UV irradiation. J Cell Biol. Cockayne syndrome group B protein has novel strand annealing and exchange activities. Cooperation of the Cockayne syndrome group B protein and poly ADP-ribose polymerase 1 in the response to oxidative stress.

Cockayne syndrome B protein stimulates apurinic endonuclease 1 activity and protects against agents that introduce base excision repair intermediates. Cockayne syndrome group B protein prevents the accumulation of damaged mitochondria by promoting mitochondrial autophagy. J Exp Med. Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging.

Iyama and Wilson Page 22 Detecting UV-lesions in the genome: The modular CRL4 ubiquitin ligase does it best! FEBS Lett. Translocation of Cockayne syndrome group A protein to the nuclear matrix: CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome.

Shining a light on xeroderma pigmentosum.

J Invest Dermatol. Xeroderma pigmentosum. Cutaneous, ocular, and neurologic abnormalities in published cases. Arch Dermatol. Neurological manifestations in xeroderma pigmentosum. Ann Neurol. Cancer and neurologic degeneration in xeroderma pigmentosum: J Med Genet. Cleaver JE. Cancer in xeroderma pigmentosum and related disorders of DNA repair. Nat Rev Cancer. Nat Neurosci. Neurological symptoms and natural course of xeroderma pigmentosum.

Xeroderma Pigmentosum and medulloblastoma: Radiat Res. Lehmann AR. Adv Exp Med Biol. Nucleotide excision repair and human syndromes. Natale V. A comprehensive description of the severity groups in Cockayne syndrome. Am J Med Genet A. Iyama and Wilson Page 23 Cockayne syndrome B mice is associated with skin cancer predisposition.

Age-related neuronal degeneration: PLoS Genet. Identification of C7orf11 TTDN1 gene mutations and genetic heterogeneity in nonphotosensitive trichothiodystrophy. Nat Genet. Nouspikel T, Hanawalt PC.

Terminally differentiated human neurons repair transcribed genes but display attenuated global DNA repair and modulation of repair gene expression. Transcription domain-associated repair in human cells. Nouspikel T.

Nucleotide excision repair and neurological diseases. Free radical-induced damage to DNA: Free Radic Biol Med. Gedik CM, Collins A. Establishing the background level of base oxidation in human lymphocyte DNA: A genome-wide distribution of 8-oxoguanine correlates with the preferred regions for recombination and single nucleotide polymorphism in the human genome. Genome Res.

Maki H, Sekiguchi M. MutT protein specifically hydrolyses a potent mutagenic substrate for DNA synthesis. Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG.

Bregeon D, Doetsch PW. Transcriptional mutagenesis: Transcriptional mutagenesis induced by 8-oxoguanine in mammalian cells.

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NUDT16 is a deoxy inosine diphosphatase, and its deficiency induces accumulation of single-strand breaks in nuclear DNA and growth arrest.

Quantification of DNA damage products resulting from deamination oxidation and reaction with products of lipid peroxidation by liquid chromatography isotope dilution tandem mass spectrometry. Nat Protoc. Dong M, Dedon PC. Relatively small increases in the steady-state levels of nucleobase deamination products in DNA from human TK6 cells exposed to toxic levels of nitric oxide.

Chem Res Toxicol. Iyama and Wilson Page 24 Variation in base excision repair capacity. Repair of persistent strand breaks in the mitochondrial genome. Mech Ageing Dev.

Demple B, Sung JS. Molecular and biological roles of Ape1 protein in mammalian base excision repair. The major human abasic endonuclease: Wilson SH. Mammalian base excision repair and DNA polymerase beta. Interaction of human apurinic endonuclease and DNA polymerase beta in the base excision repair pathway. AP endonuclease-independent DNA base excision repair in human cells. Stable down-regulation of human polynucleotide kinase enhances spontaneous mutation frequency and sensitizes cells to genotoxic agents.

Proliferating cell nuclear antigen facilitates excision in long-patch base excision repair. Protein-protein interactions and posttranslational modifications in mammalian base excision repair. A conserved interaction between the replicative clamp loader and DNA ligase in eukaryotes: Curr Biol. Extracts of proliferating and non-proliferating human cells display different base excision pathways and repair fidelity.

MUTYH-associated polyposis--from defect in base excision repair to clinical genetic testing. Human uracil-DNA glycosylase deficiency associated with profoundly impaired immunoglobulin class-switch recombination. Nat Immunol. Iyama and Wilson Page 25 Acta Neuropathol. Neurobiol Aging. XRCC1 haploinsufficiency in mice has little effect on aging, but adversely modifies exposure-dependent susceptibility. Evidence that OGG1 glycosylase protects neurons against oxidative DNA damage and cell death under ischemic conditions.

J Cereb Blood Flow Metab. Increased postischemic brain injury in mice deficient in uracil-DNA glycosylase. J Clin Invest. Defective DNA single-strand break repair in spinocerebellar ataxia with axonal neuropathy Hereditary ataxia SCAN1 cells are defective for the repair of transcription-dependent topoisomerase I cleavage complexes.

TDP1 facilitates chromosomal single-strand break repair in neurons and is neuroprotective in vivo. Hit proteins, mitochondria and cancer. Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene. Aprataxin, a novel protein that protects against genotoxic stress.

Hum Mol Genet. Nucleolar localization of aprataxin is dependent on interaction with nucleolin and on active ribosomal DNA transcription.

Protein kinase C gamma, a protein causative for dominant ataxia, negatively regulates nuclear import of recessive-ataxia-related aprataxin.

Aprataxin localizes to mitochondria and preserves mitochondrial function. A new XRCC1-containing complex and its role in cellular survival of methyl methanesulfonate treatment. Synergistic decrease of DNA single-strand break repair rates in mouse neural cells lacking both Tdp1 and aprataxin.

DNA mismatch repair. Wagner R Jr, Meselson M. Repair tracts in mismatched DNA heteroduplexes.

Iyama and Wilson Page 27 Identification and survival of carriers of mutations in DNA mismatch-repair genes in colon cancer. Jacob S, Praz F. DNA mismatch repair defects: Familial mutations in PMS2 can cause autosomal dominant hereditary nonpolyposis colorectal cancer.

Distinction of hereditary nonpolyposis colorectal cancer and sporadic microsatellite-unstable colorectal cancer through quantification of MLH1 methylation by real-time PCR. Clin Cancer Res.

Peltomaki P, Vasen H. Dis Markers. Role of hMLH1 promoter hypermethylation in drug resistance to 5-fluorouracil in colorectal cancer cell lines. Int J Cancer. Brooks PJ. DNA repair in neural cells: J Neurosci. Yanamadala S, Ljungman M. Mol Cancer Res.

Mismatch repair processing of carcinogen-DNA adducts triggers apoptosis. Role of DNA mismatch repair and p53 in signaling induction of apoptosis by alkylating agents. Msh2 status modulates both apoptosis and mutation frequency in the murine small intestine.

Mouse embryonic stem cells carrying one or two defective Msh2 alleles respond abnormally to oxidative stress inflicted by low-level radiation. Iyama and Wilson Page 28 Ionizing radiation-induced apoptosis via separate Pms2- and pdependent pathways. DNA double-strand break signaling and human disorders. Genome Integr. Jackson SP, Bartek J. The DNA-damage response in human biology and disease.

An overview of three new disorders associated with genetic instability: Impaired nonhomologous end-joining provokes soft tissue sarcomas harboring chromosomal translocations, amplifications, and deletions. The Mre11 complex: Evidence for replicative repair of DNA double-strand breaks leading to oncogenic translocation and gene amplification.

Genome maintenance mechanisms for preventing cancer. Effect of meiotic recombination on the production of aneuploid gametes in humans.

Cytogenet Genome Res. The MRE11 complex: Lavin MF. Lavin MF, Kozlov S. Cell Cycle. Yun MH, Hiom K. Factors determining DNA double-strand break repair pathway choice in G2 phase. Reconstitution of the strand invasion step of double-strand break repair using human Rad51 Rad52 and RPA proteins.

Iyama and Wilson Page 29 Kass EM, Jasin M. Shinohara A, Ogawa T. Stimulation by Rad52 of yeast Radmediated recombination. Sung P. Function of yeast Rad52 protein as a mediator between replication protein A and the Rad51 recombinase. Identification of Holliday junction resolvases from humans and yeast.

EMBO Rep. Regulation of homologous recombination in eukaryotes. Annu Rev Genet. Mechanism of eukaryotic homologous recombination. Annu Rev Biochem. Terminally differentiated astrocytes lack DNA damage response signaling and are radioresistant but retain DNA repair proficiency.

Cell Death Differ. Responding to DNA double strand breaks in the nervous system. Visualization of recombination intermediates produced by RADmediated single-strand annealing. Human Radmediated homology search and annealing occurs by continuous interactions between overlapping nucleoprotein complexes.

Lieber MR. V D J and immunoglobulin class switch recombinations: The E3 ubiquitin ligase Rnf8 stabilizes Tpp1 to promote telomere end protection. Iyama and Wilson Page 30 These findings suggested that NHEJ factors play variable, albeit critical, roles in maintaining viability of non-proliferating cells like neurons.

Iyama and Wilson Page 8 erroneous transcription can give rise to phenotypical changes with the potential to alter the fate of mammalian cells []. DSBR is divided into two major pathways: Modrich P. Lehmann AR.

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