archlibrary.com www.scholarsrese t Available online a Scholars Research Library Der Pharmacia Lettre, 2016, 8 (19):269-274 (http://scholarsresearchlibrary.com/archive.html) ISSN 0975-5071 USA CODEN: DPLEB4 269 Scholar Research Library Toxic nephropathy due to bromobenzene intoxication and the protective role of alternative medicines Udhaya Lavinya B., Asha Devi S. and Sabina E. P.* School of Biosciences and Technology, VIT University, Vellore-632014, Tamilnadu, India _____________________________________________________________________________________________ ABSTRACT Bromobenzene is an environmental toxin. Exposure to bromobenzene causes injury to hepatic and extra-hepatic tissues. The secondary metabolites of bromobenzene are toxic to kidneys. Bromobenzene is capable of causing ATP depletion, mitochondrial dysfunction, local inflammation, lipid peroxidation and subsequent loss of cellular function and integrity. This review provides insights into the mechanisms involved in bromobenzene intoxication and the effectiveness of several alternative medicines studied so far against bromobenzene-induced nephrotoxicity. Keywords: Bromobenzene, hepatotoxicity, oxidative damage, alternative medicines _____________________________________________________________________________________________ INTRODUCTION Drug-induced nephrotoxicity is seen as a common cause of many therapeutic drugs. Cases of acute renal injury have been increasingly reported since last two decades and are found to be the cause of morbidity and mortality [1]. Drugs such as aminoglycoside antibiotics, amphotericin B, non-steroidal anti-inflammatory drugs (NSAIDS), certain cyclo-oxygenase-2 (COX-2) inhibitors and angiotensin-converting enzyme inhibitors (ACEIs) have been frequently reported to cause drug-induced nephrotoxicity [2]. Drugs like rifampicin, isoniazid, anti-malarials, anti- virals, penicillin, cephalosporins, sulfonamides, aminosalicylic acid and methyldopa are capable of causing hemolysis and myoglobinuria possibly leading to renal failure [3,4]. Some of the common patient-related risk factors for drug-induced nephrotoxicity are age above 60 years, renal insufficiency, diabetes, heart failure and sepsis [5]. Apart from these therapeutic agents there are also several environmental pollutants and industrial chemicals that may lead to the development of acute and chronic kidney disease [6]. Heavy metals like cadmium, lead, chromium, uranium and mercury are also nephrotoxic. They cause toxicity in kidneys by reducing the renal blood flow thereby affection the glomerular filtration [7]. Another mechanism that has been found in metal-induced nephrotoxicity is glutathione (GSH) conjugation and in addition binding of these metals to metallothionein is also a significant process [8]. Both these mechanisms lead to bioaccumulation of these metals rather than serving as defense mechanisms. Chemicals which are halogenated hydrocarbons like trichloroethane and chloroform conjugate with GSH in the liver before they are taken up by the kidneys causing nephrotoxicity [9,10]. In particular, the anatomical features and physiological functions of the kidney make it the target organ for these toxicants upon their conjugation with GSH. This initiates different mechanisms resulting in the inhibition of renal function. Furthermore, the compounds that are not water soluble precipitate in the tubules causing obstruction in the tubular flow and subsequently cause damage to the architecture of the tubular epithelium. There may be cell death contributed by both apoptosis and necrosis in acute renal injury [11]. PHYSICO-CHEMICAL PROPERTIES OF BB Human beings are exposed to a variety of chemicals and pollutants on daily basis that result in serious health defects. Bromobenzene (BB) is a xenobiotic which is released into the environment during its production in industries. This halogenated hydrocarbon (Figure 1) has a molecular mass of 157.01 g/mol and is a colorless liquid