Incomplete combustion of polycyclic aromatic hydrocarbons (PAHs) during coal combustion, biomass burning, and automobile emissions produce hazardous materials [1]. PAHs are major components in petroleum-contaminated soils and are resistant to degradation processes thus have a strong carcinogenic effect on human health, and therefore pose a serious risk to ecosystem [2,3]. Nevertheless, exposure to PAHs has been associated with a series of adverse outcomes, including cardiovascular diseases [4], cancer [5], and type 2 diabetes [6]. Similarly, benzene is produced from cigarette smoke, urban traffic and industrial processes where human beings are frequently exposed [7,8]. Further, quinones are class of compounds that has numerous applications in the pharmaceutical and dye industries and thus exposure to human beings cannot be ignored [9]. Moreover, hydroquinone is one of the important metabolites of benzene, which is further oxidized in vivo to give para-benzoquinone (BQ). Both the metabolites are harmful to human beings than their respective parent compounds [10]. Diesel and cigarette smoke also consists of BQ which is a bioactive quinone, causing severe genotoxic effects both in vitro and in vivo. One of the key mechanisms of BQ is to damage the microtubule by inducing cytotoxity in lung cells [11]. Benzene and BQ has a strong toxic effect through acute exposure to the hematopoetic system of both laboratory animals [12,13] and leukemogenic to human beings [13,14] mostly via interaction with undifferentiated bone marrow cells. The occurrence of BQ adducts with albumin in organisms indicate that dietary and/or endogenous sources of BQ precursors are also important in the formation of such adducts [[15], [16]]. The levels of BQ-albumin adduct in the general population span a broad range, supporting the hypothesis that demographic, dietary, and lifestyle are important variables [17]. Further it was reported that DNA adducts by benzene metabolites may testify the etiological role in benzene-activated bone marrow diseases [18]. Cellular metabolism of benzene generates human leukemia carcinogen agents such as BQ [10], which can damage DNA by forming the exocyclic base adducts such as pBQ-dC, pBQ-dA, and pBQ-dG in vitro [[19], [20]]. However, the mechanisms behind such toxic outcomes are unknown, though oxidative damage and inflammation are likely to be involved in the aforesaid disorders [[1], [21], [22]]. Nevertheless, the compromised conformation of biological macromolecules cannot be ruled out by the direct interaction with BQ. With this background, the current communication aimed to examine the biophysical interaction between BQ with calf thymus DNA and human serum albumin (HSA).

HSA represents roughly 60% of the total protein content in blood [23] with a concentration of around 0.6 mM in the human plasma [24,25]. HSA is physiologically important protein which reversibly bound to a wide range of drugs and small compounds and thus modulates biochemical pathways [23]. The primary function of HSA is to control the colloidal osmotic pressure of plasma and also to maintain the pH [26]. Binding and transport of drug molecules, as well as antioxidant and anti-inflammatory properties, are some of the other physiological roles of HSA [27]. Albumin has long been used to treat a variety of medical conditions, including circulatory insufficiency. It has been well established that hypoalbuminemia is a powerful prognostic marker in the general population for many pathological settings, mainly as a result of malnutrition and inflammation [28]. Nevertheless, growing evidence suggest that low serum albumin levels are linked to the emergence of several cardiovascular diseases, such as ischemic heart disease, heart failure, atrial fibrillation, stroke, venous thromboembolism, and inflammation [29]. Moreover, albumin is useful in detoxification reactions, as well as in the activation of prodrugs and drug conjugates [30]. The impaired transport of drugs, hormones, and metabolites associated with altered structure of HSA has been reported to contribute towards various metabolic syndromes [23], however more extensive studies are required for a conclusive interpretation. On the other hand, the blue print of life stored in DNA guides the biological synthesis of proteins and enzymes through transcription and translation. Moreover, cell functions are regulated by modulating transcription or by interfering with replication through targeting DNA. Small ligand molecules can alter or inhibit the function of DNA by covalent or non-covalent interactions [31,32]. The chemico-biological interactions between ligands and biomacromolecules is not only demonstrate the mechanism of interactions but also decipher the ligand-induced possible pathophysiological consequences. Thus, interaction of BQ with DNA and HSA was carried out using various biophysical techniques and computational tools.