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Nayak P.,NRI Medical College and General Hospital | Sharma S.B.,Chettinad Hospital and Research Institute | Chowdary N.V.S.,NRI Medical College and General Hospital
Neurochemical Journal | Year: 2012

Cerebellum is unique in restraining amyloid-induced neurodegenerative changes. Amyloidosis and oxidant imbalance is common in aluminum exposure. Interestingly, aluminum itself does not pose any redox activity still it is associated with oxidant imbalance, and, it can aggravate the situation of already existing oxidant threat. Male rats were exposed to aluminum for 4 weeks along with exposure to 4 different doses of ethanol. After the treatment period, cerebellar level of protein, reduced glutathione (GSH), lipid perioxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) were also estimated from the homogenized cerebellar tissue. In the present regimen of aluminum exposure, the cerebellum has shown significant reduction only in GPx activity. However, when aluminum was coexposed with ethanol, it contributed significantly to increase the cerebellar oxidant imbalance by (a) compromising the GSH restoration system, (b) reducing enzymatic peroxide scavenging system of cerebellum, (c) restricting the capability to cope with oxidative stress, as well as (d) downgrading the resistance to oxidative damage in response to chemical stress. Present study demonstrates that coexposure of aluminum with pro-oxidant favored development of aluminum-induced oxidative stress in cerebellum. These observations enlighten the role of pro-oxidants in the process of oxidative degeneration of cerebellum. With further studies, the present observation can be useful to understand the mechanism of neurodegenerative disorders and ways to ameliorate them. © 2012 Pleiades Publishing, Ltd. Source


Sangam M.R.,NRI Medical College and General Hospital | Anasuya K.,NRI Medical College and General Hospital
Folia Morphologica | Year: 2010

We report a case of left sided aortic arch with three branches -a bi-carotid trunk, left subclavian, artery and right subclavian artery. The anomalous right subclavian artery presented a retroesophageal course. A right non-recurrent laryngeal nerve was noticed. The embryonic development of this branching pattern is discussed. Copyright © 2010 Via Medica. Source


Nayak P.,NRI Medical College and General Hospital | Sharma S.B.,Chettinad Hospital and Research Institute | Chowdary N.V.S.,NRI Medical College and General Hospital
Indian Journal of Experimental Biology | Year: 2015

Superoxide and peroxide handling capacity (SPHC) is an important determinant of oxidative stress. Neurotoxic impacts of aluminum are associated with oxidant imbalance. Here, we studied the influence of aluminum on oxidative stress parameters, antioxidative enzymes and SPHC of thalamic area on pro-oxidant (ethanol) and antioxidant (α-tocopherol) exposure. Two sets of male Wistar rats were divided into 8 groups (6 each) and exposed to aluminum (10 mg/Kg body wt.), ethanol (0.6 g/Kg body wt.) and α-tocopherol (5 IU/day) for 4 wk, each having respective control group. Levels of reduced glutathione (GSH), lipid peroxidation (TBARS) along with activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) of thalamic area were estimated for each group. Glutathione-independent superoxide peroxide handling capacity (GI-SPHC) and glutathione-dependent superoxide peroxide handling capacity (GD-SPHC) were calculated from the GPx, CAT and SOD values. Concomitant exposure to aluminum and ethanol demonstrated significant increase in SOD activity and significant decrease in GPx activity compared to the control group, while lone aluminum-exposed rats showed raised GR activity, without alterations in GPx and SOD activities. However, significant reduction of both GI- and GD- SPHC were found in ethanol-exposed groups. α-Tocopherol supplementation could resist most of the alterations. In addition, current antioxidant exposure reduced the inherent GD-SPHC, and thus, made thalamic area more vulnerable to oxidant threat. The present study corroborates the thalamic susceptibility to aluminum-augmented oxidant imbalance and suggests cautious use of antioxidant supplementation against neurodegenerative disorders. © 2015, National Institute of Science Communication. All rights reserved. Source


Koti K.,NRI Medical College and General Hospital | Gunnamreddy R.,NRI Medical College and General Hospital
Indian Journal of Dermatology | Year: 2013

Encephalocraniocutaneous lipomatosis (ECCL) is a rare sporadic neurocutaneous syndrome characterized by presence of central nervous system, ocular and cutaneous anomalies. The exact pathogenesis is still not known. We present the third case from the Indian subcontinent, who is a five year old girl with history of right sided seizures. Dermatological examination showed alopecia on right side of the scalp and ipsilateral limbal dermoid and nodular skin tags over the upper eyelid. The computerized tomography scan of the brain revealed porencephalic cyst, cerebral calcifications and atrophy of right brain. The histopathology of the skin lesions showed lipomatous hamartoma and features of non scarring alopecia. The constellation of these findings and in adherence to the diagnostic criteria of ECCL proposed in 2009, we consider this report as a definite case of ECCL. © Indian Journal of Dermatology 2013. Source


Nayak P.,NRI Medical College and General Hospital | Sharma S.,Chettinad Hospital and Research Institute | Chowdary N.,NRI Medical College and General Hospital
Journal of Medical Biochemistry | Year: 2011

Ubiquitous presence along with uncontrolled use of aluminum and increasing trends of ethanol consumption in India increased the chance of coexposure to aluminum and ethanol. Possibilities are there, that both of them follow common mechanisms to produce neurotoxicity. The phosphomonoesterases and glutamate transaminases are studied in rat brain cerebrum after combined exposure to aluminum and varied doses of ethanol for 4 weeks. Dose dependent decreases in growth have been observed. The impact of aluminum on cerebral acidic and alkaline phosphomonoesterases activities were shown to be altered in a dose dependent fashion by the coexposure to ethanol. Aspartate aminotransferase and alanine aminotransferase of the cerebrum were responding differentially to aluminum exposure in the presence of different doses of ethanol exposure. It has been suggested that the ethanol-induced augmentation of impacts of aluminum on the cerebrum is dose dependent and there might be a critical level of ethanol exposure for the observed effect on cerebrum. Source

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