Senthamilselvan Bavithra

Polychlorinated biphenyls induced oxidative stress mediated neurodegeneration in hippocampus and behavioral changes of adult rats: anxiolytic-like effects of quercetin.

Polychlorinated biphenyls (PCBs) are extremely toxic environmental contaminant speculated to accelerate neurochemical and behavioral damages. Developmental and behavioral development relies on the proper functioning of the endogenous neurotransmitters that remain the pivotal target of neurotoxicants. This study intent to evidence the neuroprotective efficacy of quercetin against PCBs induced hippocampal degeneration. Animals were sorted into four (n=6), Group I: received corn oil (vehicle) intraperitoneally (i.p.); Group II: received quercetin 50 mg/kg bwt (gavage); Group III: were induced with Aroclor 1254 (commercial mixture of PCB) at 2 mg/kg bwt (i.p); Group IV: received quercetin 50 mg/kg bwt (gavage) and along with PCBs 2 mg/kg bwt (i.p.) for 30 days. Cognitive behaviors such as learning and memory were assessed by 8-arm radial maze behavior test throughout the experimental period. Subsequently, anxiety and stress were studied by open field test at the termination of experiment. Hippocampal tissue and blood were collected after the intended experimental period to analyze the levels of oxidative stressors, antioxidants in tissue and estimation of neurotransmitters. Perhaps, PCBs evoke detrimental deterioration of the neurotransmitters and integrative antioxidant defense by elevation of reactive oxygen species (ROS). Concurrent treatment with quercetin prominently suppresses the oxidative stressors, improved the levels of enzymatic antioxidants and neurotransmitter levels significantly at the level of p<0.05. Behavioral analysis claims drastic revitalization of cognitive functions like learning and memory on treatment with quercetin. The results coalesced depicts neurotoxicity stimulated by PCBs is augmented by simultaneous quercetin administration.

Polychlorinated biphenyls-induced oxidative stress on rat hippocampus: a neuroprotective role of quercetin.

Present study is aimed to evaluate the ameliorative role of quercetin on PCBs-induced oxidative stress in hippocampus of Wistar rats. Group I rats received vehicle (corn oil) intraperitoneally (i.p); Group II received quercetin 50 mg/kg bwt/day (gavage); Group III received PCB 2 mg/kg bwt/day (i.p); Group IV received PCB (i.p) and simultaneously quercetin through gavage. After 30 days, rats were euthanized and hippocampus was dissected from each rat brain. Oxidative stress was assessed by determining the levels of H2O2, LPO, Pcc, and alteration in the functional markers such as CK, AchE, and ATPases activities in the hippocampus of control and experimental animals. A significant increase in the levels of stress markers and decrease in level of functional markers were observed in PCBs-treated rats. Moreover DNA fragmentation and histological studies were ascertained to confirm PCBs toxicity. In conclusion, quercetin shows a protective role against PCBs-induced oxidative damage in rat hippocampus.

Effect of Quercetin on Haematobiochemical and Histological Changes in the Liver of Polychlorined Biphenyls-Induced Adult Male Wistar Rats

Polychlorinated biphenyls exposure damages the rat liver cells. Hematological parameters such as hemoglobin, packed cell volume, red-blood cells, white-blood cells, neutrophils, platelet counts, and RBC indices were significantly decreased. Polymorphs, eosinophil counts, and erythrocyte sedimentation rate were significantly increased. Serum liver enzymes such as aspartate transaminase, alanine transaminase, alkaline phosphatase, and gamma-glutamyl transferase were increased by PCBs treatment. Serum lipid profiles such as cholesterol, triglycerides, low-density lipoproteins and very-low-density lipoproteins were increased in PCBs-treated rats. High-density lipoprotein, total protein, albumin, globulin levels, and albumin/globulin ratio were also decreased after PCB exposure. Then levels of sodium, potassium, chloride, and bicarbonate were also altered. Serum glucose levels were increased along with total bilirubin after PCBs exposure. Simultaneous quercetin supplementation significantly protected the PCBs-induced changes of hematobiochemical parameters. Thus, quercetin shows a protective role against PCBs-induced alterations in the hematological and biochemical parameters.

Melatonin attenuates polychlorinated biphenyls induced apoptosis in the neuronal cells of cerebral cortex and cerebellum of adult male rats--in vivo.

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.

Neuroprotective Effect of Melatonin Against PCBs Induced Behavioural, Molecular and Histological Changes in Cerebral Cortex of Adult Male Wistar Rats.

There is ample evidence stating Polychlorinated biphenyls (PCBs) as neurotoxins. In the current study, we have analyzed the behavioural impact of PCBs exposure in adult rats and assessed the simultaneous effect of antioxidant melatonin against the PCBs action. The rats were grouped into four and treated intraperitoneally with vehicle, PCBs, PCBs + melatonin and melatonin alone for 30 days, respectively. After the treatment period the rats were tested for locomotor activity and anxiety behaviour analysis. We confirmed the neuronal damage in the cerebral cortex by molecular and histological analysis. Our data indicates that there is impairment in locomotor activity and behaviour of PCBs treated rats compared to control. The simultaneous melatonin treated rat shows increased motor coordination and less anxiety like behaviour compared to PCBs treated rats. Molecular and histological analysis supports that, the impaired motor coordination in PCBs treated rats is due to neurodegeneration in motor cortex region. The results proved that melatonin treatment improved the motor co-ordination and reduced anxiety behaviour, prevented neurodegeneration in the cerebral cortex of PCBs-exposed adult male rats.