Background: Lactate dehydrogenase (LDH) is a group of oxidoreductase isoenzymes catalyzing the reversible reaction between pyruvate and lactate. The five isoforms of this enzyme, formed from two subunits, vary in isoelectric points and these isoforms have different substrate affinity, inhibition constants and electrophoretic mobility. These diverse biochemical properties play a key role in its cellular, tissue and organ specificity. Though LDH is predominantly present in the cytoplasm, it has a multi-organellar location as well. Objective: The primary objective of this review article is to provide an update in parallel, the previous and recent biochemical views and its clinical significance in different diseases. Methods: With the help of certain inhibitors, its active site three-dimensional view, reactions mechanisms and metabolic pathways have been sorted out to a greater extent. Overexpression of LDH in different cancers plays a principal role in anaerobic cellular metabolism, hence several inhibitors have been designed to employ as novel anticancer agents. Discussion: LDH performs a very important role in overall body metabolism and some signals can induce isoenzyme switching under certain circumstances, ensuring that the tissues consistently maintain adequate ATP supply. This enzyme also experiences some posttranslational modifications, to have diversified metabolic roles. Different toxicological and pathological complications damage various organs, which ultimately result in leakage of this enzyme in serum. Hence, unusual LDH isoform level in serum serves as a significant biomarker of different diseases. Conclusion: LDH is an important diagnostic biomarker for some common diseases like cancer, thyroid disorders, tuberculosis, etc. In general, LDH plays a key role in the clinical diagnosis of various common and rare diseases, as this enzyme has a prominent role in active metabolism.

Cinnamaldehyde, a food flavour, has a high potential for human consumption in India. In this study, we evaluated the effect of cinnamaldehyde on the antioxidant status of the rat kidney. Rats were given cinnamaldehyde orally by gavage at dose levels of 2.14, 6.96, 22.62 and 73.5 mg/kg body weight/day for the period of 10, 30 and 90 days. The non-enzymatic antioxidants ascorbic acid, a-tocopherol and reduced glutathione were decreased while the antioxidant enzymes, superoxide dismutase, glutathione peroxidase and glutathione-s-transferase were increased. Catalase was decreased and thiobarbituric acid-reactive substances were increased only in the kidney of rats treated with cinnamaldehyde at the dose level of 73.5 mg/kg body weight/day during an exposure period of 90 days and not in the kidney of other cinnamaldehyde-treated rat groups. Thus, cinnamaldehyde has an effect on the antioxidant status of rat kidney and its effect is time-and dose-dependent.

Bisphenol A (BPA), the highest volume chemical produced in the whole world is widely used in the production of polycarbonate plastics and epoxy resins. Polycarbonate plastics are used especially in the manufacture of consumer products. The exposure of BPA to humans occurs through food contamination from polycarbonate bottles and food and beverage cans. Dust is also a contributor to the total daily exposure of BPA. Thus, BPA has a high potential for human consumption. The U.S. Food and Drug Administration (FDA) recently announced concern about the safety of BPA and the need for more research data. This article reviews toxicity of BPA in general and kidney in particular using clinical and experimental literature. BPA is toxic to aquatic organisms, animals and humans. BPA is cytotoxic and mutagenic and exerts various adverse effects on immune, endocrine, reproductive, developmental and nervous systems in animals and human and exhibits toxicity by all routes of exposure. Metabolism of BPA is much more rapid in humans than in rodents. BPA increases estrogen metabolism in the kidney and upregulates cytochrome p-450 aromatase activity by means of steroidogenesis. BPA acts as biomarker for renal disease and exhibits nephrotoxicity. BPA toxicity with reference to human exposure level and also carcinogenicity are lacking. While focusing on kidney, this review suggests that further research is required to evaluate the molecular mechanism of BPA induced nephrotoxicity. Protective role of antioxidants against BPA induced toxicity / nephrotoxicity is discussed in this literature.

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