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Kowsalya V.,Sri Lakshmi Narayana Institute of Medical science | Vijayakumar R.,Sri Lakshmi Narayana Institute of Medical science | Valli G.,Meenakshi University | Bharath K.P.,Asan Memorial Dental College and Hospital | And 4 more authors.
Pakistan Journal of Biological Sciences | Year: 2013

Birth weight is an important determinant of child survival, healthy growth and development. Low birth weight is a well-established risk factor for adverse long term health, particularly cardiovascular disease and metabolic syndrome. The ability of the fetus to grow and thrive in utero is presumed to be a function of the placenta. The present study was aimed to assess the morphometry examination of placenta in normal and low birth weight babies in the Union territory of Puducherry. Morphometry examination includes Placenta weight, number of cotyledons, maternal and fetal surface area and site of umbilical cord insertion were measured in normal and low birth weigh babies. Result showed among 200 subjects, mean birth weight of normal and low birth babies were 2806 and 2058 g, respectively. The prevalence rate of low birth babies (less than 2500 g) was 22%. The placental morphometry study namely placental weight, number of cotyledons, maternal and fetal surface area and insertion of umbilical cord at centre were significantly (p<0.001) reduced in the low birth weight babies when compared with normal birth weight babies. Study revealed that morphometry analysis of placenta significantly influences the birth weight of new born. In conclusion, study recommends the early measurements of placenta by non-invasive techniques like ultrasonography will be helpful in early prediction of low birth weight fetus in utero itself and for better management to avoid such low birth weight. © 2013 Asian Network for Scientific Information. Source


Bavithra S.,University of Madras | Selvakumar K.,University of Madras | Krishnamoorthy G.,Asan Memorial Dental College and Hospital | Venkataraman P.,SRM University | Arunakaran J.,University of Madras
Environmental Toxicology and Pharmacology | Year: 2013

Polychlorinated biphenyls (PCBs) are widespread persistent environmental contaminants that display a complex spectrum of toxicological properties, including neurotoxicity. Studies have shown that PCBs increase oxidative stress in brain, leading to apoptosis. The progressive loss of neurons in cerebral cortex and cerebellum, leads to various neurodegenerative diseases. Hence the present study is designed to determine PCBs toxicity toward neuronal cells and whether it could be inhibited by potent antioxidant melatonin. Four groups of adult male Wistar rats were treated for 30 days with corn oil, PCBs, PCBs. +. Mel and Melatonin, respectively. After treatment period the rats were euthanized and the brain was dissected to isolate cerebral cortex and cerebellum. The neuronal cells alone were then separated from the isolated brain regions, to detect the mRNA levels of apoptotic and neurofilament gene, a neuronal specific marker. Our results suggests that PCBs induces apoptosis in neuronal cells which is subsided by the anti apoptotic effect of melatonin. © 2013 Elsevier B.V. Source


Selvakumar K.,University of Madras | Prabha R.L.,University of Madras | Saranya K.,University of Madras | Bavithra S.,University of Madras | And 2 more authors.
Human and Experimental Toxicology | Year: 2013

Polychlorinated biphenyls (PCBs) comprise a ubiquitous class of toxic substances associated with carcinogenic and tumor-promoting effects as well as neurotoxic properties. Reactive oxygen species, which is produced from PCBs, alters blood-brain barrier (BBB) integrity, which is paralleled by cytoskeletal rearrangements and redistribution and disappearance of tight junction proteins (TJPs) like claudin-5 and occludin. Quercetin, a potent antioxidant present in onion and other vegetables, appears to protect brain cells against oxidative stress, a tissue-damaging process associated with Alzheimer's and other neurodegenerative disorders. The aim of this study is to analyze the role of quercetin on oxidative stress markers and transcription of transmembrane and cytoplasmic accessory TJPs on cerebrum, cerebellum and hippocampus of female rats exposed to PCBs. Rats were divided into the following four groups. Group I: received only vehicle (corn oil) intraperitoneally (i.p.); group II: received Aroclor 1254 at a dose of 2 mg/kg body weight (bwt)/day (i.p); group III: received Aroclor 1254 (i.p.) and simultaneously quercetin 50 mg/kg bwt/day through gavage and group IV: received quercetin alone gavage. From the experiment, the levels of hydrogen peroxide, lipid peroxidation and thiobarbituric acid reactive substances were observed to increase significantly in cerebrum, cerebellum and hippocampus as 50%, 25% and 20%, respectively, after exposure to PCB, and the messenger RNA expression of TJP in rats exposed to PCBs is decreased and is retrieved to the normal level simultaneously in quercetin-treated rats. Hence, quercetin can be used as a preventive medicine to PCBs exposure and prevents neurodegenerative disorders. © 2013 The Author(s). Source


Selvakumar K.,University of Madras | Bavithra S.,University of Madras | Suganthi M.,University of Madras | Benson C.S.,University of Madras | And 5 more authors.
Neurochemical Research | Year: 2012

Polychlorinated biphenyls (PCBs) exposure produces neurodegeneration and induces oxidative stress. Neuroprotective role of quercetin, on PCBs induced apoptosis in hippocampus has not yet been studied. The present study is focused to see whether quercetin supplementation precludes against PCBs induced oxidative stress and hippocampal apoptosis. The results have shown that quercetin at 50 mg/kg bwt/30 days has protected oxidative stress in hippocampus of adult male rats. Quercetin, a free radical scavenger decreased the levels of oxidative stress markers in the hippocampus of simultaneous PCB+quercetin treated rats. The pro-apoptotic and anti-apoptotic molecules such as Bad, Bid, Bax and Bcl2 were altered in the hippocampus of experimental animals. PCBs increased the DNA damage and induced neurodegeneration were assessed by histological studies. PCB induced ROS may be linked to increased hippocampal neuronal apoptosis. Quercetin supplementation decreased the neuronal damage and scavenged the free radicals induced by PCBs and protects PCBs induced apoptosis and oxidative stress. © Springer Science+Business Media, LLC 2011. Source


Bala Sakthi Janani M.M.,University of Madras | Selvakumar K.,University of Madras | Suganya S.,University of Madras | Fariya Yasmine A.B.,University of Madras | And 2 more authors.
Biomedicine and Aging Pathology | Year: 2012

Polychlorinated biphenyls (PCBs) are known to be putative environmental toxin that produce neurotoxicity and also affect reproductive and endocrine functions. PCBs induce the production of reactive oxygen species (ROS) leading to oxidative stress induced neuronal damage. This study is designed to examine the production of reactive nitrogen species (RNS) by PCB exposure and to validate the alleviating effect of lycopene, a potent dietary anti-oxidant on marker enzymes and protein affected by nitrosative stress induced by PCBs in cerebral cortex of adult male rats. Rats were divided into four groups of six each. Group I rats intraperitoneally (i.p.) administered corn oil (vehicle); group II received lycopene 4 mg/kg/bwt (gavage); group III received PCBs (Aroclor 1254) at 2 mg/kg bwt (i.p); group IV received lycopene 4 mg/kg bwt (gavage) and simultaneously with PCBs 2 mg/kg bwt (i.p.). The treatment was given daily for 30 days. Twenty-four hours after the experimental period rats were euthanized. From each rat cerebral cortex tissues was collected and analyzed for mean activities of marker enzymes acetyl cholinesterase (AchE) and creatine kinase (CK). The fate of the mRNA expression of neuronal nitric oxide synthase (nNOS), protein expression of 3-nitro-tyrosine and concentration of nitrite level were analyzed. Results proclaim that PCB induces nitrosative stress in cerebral cortex via RNS production and lycopene acts as a potent anti-oxidant by quenching the RNS thereby reducing the nitrosative stress and protecting from neuronal damage. © 2012 Elsevier Masson SAS. Source

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