International Journal of Medical Sciences

Kuldip Singh ¹, Arvind Preet Kaur ²

Affiliations
1 Department of Biochemistry, Government Medical College Campus, Amritsar Punjab, IN
2 Krishi Vigyan kendra, Shamsher Nagar sirhind, Fatehgarh Sahib Punjab, IN

Abstract

Reactive oxygen species occur continuously in all the cells as a part of normal cellular function. These reactive oxygen species are a potential double -edged sword in diseases prevention and promotion. The most common reactive oxygen species are hydrogen peroxide, superoxide ion and hydroxide radical are the compounds, when present in a high enough concentration, can damage cellular proteins, lipids and nucleic acids that may promote various diseases. Advances in research have shown that low to moderate concentrations of reactive oxygen species play crucial roles in normal physiological processes, such as through redox regulation of protein phosphorylation, ion channels and transcription factors etc. and are also required for biosynthetic processes, including thyroid hormone production and cross linking of extracellular matrix. Reactive oxygen species induced disease, can be either due to a lack of reactive oxygen species (e.g., chronic granulomatous disease, certain autoimmune disorders) or a surplus of reactive oxygen species (e.g., cardio-vascular and neurodegenerative diseases). The human body has several mechanisms to counteract the reactive oxygen species by producing antioxidants, which are either naturally produced in situ or externally supplied through foods and /or supplements. Antioxidant supplementation has proven largely ineffective in clinical studies, most probably because their action is too late, too little and too nonspecific. This article reviews the basic chemistry, mechanisms of formation and catabolism of reactive oxygen species, their beneficial effects and the consequences of free radical induced diseases in the body.

Keywords

Reactive Oxygen Species (ROS), Free Radicals, Antioxidants, Cancer, Cardio-vascular Disease (CVD)

Full Text

     

Kuldip Singh ¹, Arvind Preet Kaur ², Pushpa Ahluwalia ³

Affiliations
1 Department of Biochemistry, Govt. Medical College, Amritsar (Punjab), IN
2 Department of Horticulture, Punjab Agricultural University, Ludhiana (Punjab), IN
3 Department of Biochemistry, Punjab University, Chandigarh (U.T.), IN

Abstract

Monosodium glutamate (MSG) was orally administered at dose levels of 4 and 8mg/g body weight to hypercholestremic adult male mice for 6 consecutive days and its effect was observed on 31st day after the last injection by evaluating the changes in total-sulfhydryl (TSH) group, Non-protein bound sulfhydryl (NPB-SH) group and protein bound sulfhydryl (PB-SH) and glutathione metabolising enzymes like glutathione reductase (GR) and glutathione peroxidase (GPx) enzymes in cardiac tissue of hypercholestremic adult male mice. The animals were divided in four groups each comprising 6 mice. Group-I: Control, Group-II: Hypercholestremic animals, Group-III: 4mgMSG/g body weight + hypercholestremic animals and Group-IV: 8mgMSG/g body weight + hypercholestremic animals. Animals were fasted overnight and sacrificed by decapitation. The 10 per cent homogenate was prepared in 100mM potassium phosphate buffer (pH7.5). The homogenate was centrifuged at 1,000g and supernatant was used for the estimation of TSH, NPB-SH, PB-SH, GR and GPx. The levels of TSH, PBSH and NPBSH groups were significantly decreased in cardiac tissue of all the study groups. The glutathione metabolising enzymes such as GR and GPx was significantly decreased in cardiac tissue of hypercholestremic adult male mice's without MSG (Group-2) and with MSG (Group-3 and group-4) ingestion. These observations suggested that ingestion of MSG at dose levels of 4 and 8mg/g body weight to hypercholestremic animals had no beneficial effect instead it further weakens the antioxidant status in the cardiac tissue by significantly lower the levels of glutathione and its metabolising enzymes and thereby being responsible for the initiation of coronary heart disease/atherosclerosis.

Keywords

Monosodium Glutamate, Hypercholestremia, Coronary Heart Disease, Glutathione.

Full Text