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The present study was focused upon emancipating the efficacy of aqueous extract of Ipomoea batatas in abatement of bisphenol A (BPA)-induced experimental testicular toxicity. In vivo strategy of the present analysis encompasses intoxication of reproductive toxicant bisphenol A to adult male Sprague Dawley rats. Adult male Sprague Dawley rats were divided into four groups. Group I: Control, Group II: BPA-induced testicular toxicity rats (200 mg/kg body weight/day orally for 30 days), Group III: BPA-induced rats were treated with aqueous extract of I. batatas (400 mg/kg body weight/day orally for 45 days), Group IV: Normal rats treated with I. batatas aqueous extract (400 mg/kg body weight/day orally for 45 days). Marker enzymes, lipid peroxidation, and reactive oxygen species levels were found to be raised in BPA-induced testicular toxicity. Conversely, enzymatic and non-enzymatic antioxidants, mitochondria TCA cycle enzymes levels were significantly reduced. Histological changes in testis of rats ...

Colon cancer is considered as the precarious forms of cancer in many developed countries, with few to no symptoms; the tumor is often diagnosed in the later stages of cancer. Monoterpenes are a major part of plant essential oils found largely in fruits, vegetables and herbs. The cellular and molecular activities show therapeutic progression that may reduce the risk of developing cancer by modulating the factors responsible for colon carcinogenesis. Colon cancer was induced with DMH with a dose of (20 mg/Kg/body weight) for 15 weeks by subcutaneous injection once in a week. Myrtenal treatment was started with (230 mg/Kg/body weight) by intragastric administration, one week prior to DMH induction and continued till the experimental period of 30 weeks. The Invivo results exhibit the elevated antioxidant and lipid peroxidation levels in DMH treated animals. The Histopathological analysis of colon tissues well supported the biochemical alterations and inevitably proves the protective role of Myrtenal. Treatment with myrtenal to cancer bearing animals resulted in a remarkable increase in the inherent antioxidants and excellent modulation in the morphological and physiological nature of the colon tissue. It is thus concluded that myrtenal exhibits excellent free radical scavenging activity and anticancer activity through the suppression of colon carcinoma in Wistar albino rats.

Breast cancer is the most prevalent malignant neoplasm in the world, and chemoprevention through dietary intervention strategy is an emerging option to reduce the incidence. D-pinitol (DP), a major component of soya bean, possesses attractive biological actions. We have investigated whether D-pinitol have an effect on tumor growth in vivo against 7,12-dimethylbenz(a)anthracene (DMBA)-initiated rat mammary carcinogenesis and investigated its mechanism of action. Tumors were induced in Sprague-Dawley (SD) rats by a gastric dose of 20 mg/kg DMBA, and after 13 weeks of induction period, the rats were orally administered with D-pinitol for 45 days. At the end of the assay, animals in carcinogen control group prompted a tumor incidence of 100 % and developed a tumor volume of 8.35 ± 0.56, which was significantly reduced to 5.74 ± 0.32 for the animals treated with D-pinitol. The D-pinitol treatment not only decreased the tumor volume but also further examination revealed that tumors from animals that received D-pinitol reduced nuclear factor kappa B (NF-κB) activation which in turn results in modulation of its downstreaming p53 and proteins of caspase-3 family. Bcl-2 expression and caspase-3 activation were also decreased after D-pinitol supplementation leading to induction of apoptosis and finally cell death. Furthermore, the status of the inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-2, IL-6, and tumor markers, lipid profile, and hormones was also significantly declined up on D-pinitol administration. Thus, it reveals the collective involvement of the above-mentioned parameters along with NF-κB signaling through which D-pinitol induces apoptosis and subsequently suppresses breast cancer during DMBA-induced rat breast carcinogenesis.

Objective To investigate whether D-pinitol efficiently scavenge free radicals using various in vitro models [1, 1-diphenyl-2-picrylhydrazyl (DPPH), nitric oxide, superoxide anion and total antioxidant activity] and in vivo models. Methods Female Sprague-Dawley rats (150-160 g) were divided into four groups and each group consisting of six animals. Group I and group IV were vector and drug control. The group II and group III animals were treated with 7, 12-dimethylbenz(a)anthracene (DMBA) 20 mg/kg body weight to induce mammary carcinoma. Rats received cancer bearing Group III animals were treated with D-pinitol at the concentration of 200 mg/kg bodyweight for 45 d orally. Five different concentrations of D-pinitol (100 to 500 μg/mL) were used in in vitro studies. Resutls The results revealed that D-pinitol efficiently scavenges DPPH radicals and the IC50 was found to be 290 μg/mL and it also exhibited a dose dependent antioxidant activity at different concentrations. In addition, the superoxide and nitricoxide radicals were also significantly inhibited by D-pinitol at the concentrations of 360 and 390 μg/mL respectively. On the other hand, D-pinitol has significantly increased antioxidant enzymes during DMBA induced mammary carcinoma. Conclusions It can be concluded from the investigation that D-pinitol has an excellent antioxidant activity which could be due to the scavenging capacities on the stable DPPH radicals, superoxide, nitric oxide and DMBA induced free radicals thereby it exhibits remarkable total antioxidant activity.

Development of drugs from natural products has been undergoing a gradual evoluation. Many plant derived compounds have excellent therapeutic potential against various human ailments. They are important sources especially for anticancer agents. A number of promising new agents are in clinical development based on their selective molecular targets in the field of oncology. D-pinitol is a naturally occurring compound derived from soy which has significant pharmacological activitites. Therefore we selected D-pinitol in order to evaluate apoptotic potential in the MCF-7 cell line. Human breast cancer cells were treated with different concentrations of D-pinitol and cytotoxicity was measured by MTT and LDH assays. The mechanism of apoptosis was studied with reference to expression of p53, Bcl-2, Bax and NF-kB proteins. The results revealed that D-pinitol significantly inhibited the proliferation of MCF-7 cells in a concentration-dependent manner, while upregulating the expression of p53, Bax and down regulating Bcl-2 and NF-kB. Thus the results obtained in this study clearly vindicated that D-pinitol induces apotosis in MCF-7 cells through regulation of proteins of pro- and anti-apoptotic cascades.

The kidney is an imperative intention of the toxicity of drugs, xenobiotics, and oxidative stress. The intend of the present investigation was to conclude nephro-protective efficiency over mercuric chloride (MgCl2) induced oxidative stress and renal injury in rats. Mercuric chloride induced nephrotoxicity (1 mg kg bw; i.p.) as it induces noticeable and characteristic changes in proximal tubular cells in group II animals. These changes are conduit and accompanied by signs of renal dysfunctions. The levels of blood urea, serum creatinine, uric acid, and lipid peroxidation were elevated (P < 0.05) in heavy metal intoxicated group II animals. On the other hand there was a decline in the levels of serum protein, nucleic acids, enzymic and non-enzymic antioxidant enzymes in group II toxicity induced rats. In group III, rats administration of kaempferol (100 mg kg bw p.o.) brought back these elevated urinary constituents, lipid peroxidation (P < 0.05) and increase the levels of antioxidants and nucleic acids levels to near normal (P < 0.05) due to its therapeutic and scavenging properties. Histopathological results muscularly supports the nephro-protective activities of kaempferol by convalescing oxidative damage and morphological changes of kidneys induced by MgCl2. Therefore, the present analysis evidently showed that kaempferol may be useful due to antioxidant possessions in fighting against free radical-induced oxidative stress and tissue injury resulted from mercuric chloride induced nephrotoxicity.

Cadmium (Cd) is a non-essential transition metal widely distributed in the environment as a pollutant and has been shown to induce health hazards by having carcinogenic, mutagenic, teratogenic and cytotoxic effects. Exposure of human populations to cadmium from air, food and water may produce toxic effects in organs such as the kidneys, liver, lungs, cardiovascular, immune and reproductive systems. Since Cd has been identified as a human carcinogen, biomarkers for early detection of susceptibility to cancer are of an importance to public health. The ability to document Cd exposure and uptake of this element through biological monitoring is a first step towards understanding its health effects. The present study has been designed to investigate the protective role of fucoxanthin (Fxn), on cadmium chloride-induced oxidative stress and renal dysfunction in rats by analyzing the biochemical key enzymes and histopathological studies. The results revealed that administration of cadmium chloride significantly induced the renal dysfunction which was evident from the increased levels of serum blood urea nitrogen, creatinine, lipid peroxidation and concurrently the antioxidants enzymes levels of superoxide dismutase, glutathione peroxidase, reduced glutathione was significantly decreased. Interestingly, on administration of fucoxanthin along with cadmium chloride-intoxicated rats were found a significant decrease in the levels of blood urea nitrogen, creatinine, lipid peroxidation and an increase in the levels of renal antioxidant enzymes which inevitably confirms that Fxn has a prominent role in preventing the renal damage during treatment. Further histopathological examination revealed that cadmium-induced renal tissue damage was reduced by Fxn treatment. Our results suggest that Fxn reduces the cadmium-induced oxidative renal dysfunction in rats.

The aim of this study was to document the effect of hesperidin on the key enzyme activities of carbohydrate metabolism, lipid profile, and membrane-bound adenosine triphosphatases (ATPases) during 7,12-dimethylbenz( a)anthracene (DMBA)-induced breast carcinogenesis. Hesperidin has been reported to have multiple biological properties. Breast cancer was induced by single dose of DMBA (20 mg/kg body weight (bw)). The results revealed that there was a significant increase in the activities of hexokinase, phosphoglucoisomerase, and aldolase and a concomitant decrease in the activities of glucose-6-phosphatase and fructose-1,6-diphosphatase in cancer-induced animals. The activities of ATPases were found to be decreased both in erythrocyte membrane and in the liver of mammary cancer-bearing animals. The lipid profiles such as total cholesterol, free cholesterol, phospholipids, triglycerides, and free fatty acids significantly increased and in contrast the ester cholesterol in plasma was found to be decreased, whereas it was found to be elevated in the liver of cancer-bearing groups. The altered levels of the above-mentioned biochemical parameters in cancer-bearing animals were significantly ameliorated by the administration of hesperidin at the dosage of 30 mg/kg bw for 45 days. The histopathological analysis of breast and liver tissues were well supported the modulatory property of hesperidin, and this might be associated with normalizing the gluconeogenesis process, stabilization of cell membranes, and modulation of lipid biosynthesis.

Dietary compounds are reported to have the innate ability to interfere several diseases. D-Pinitol is one of the compounds from dietary origin, well documented for its excellent biological activities. We have reported the therapeutic efficiency of the D-Pinitol with reference to lipid peroxidation, antioxidants, drug metabolizing enzymes and expressions of proteins such as p53, Bcl-2, and caspase-3 during DMBA-induced mammary carcinogenesis. D-Pinitol at the dose of 200 mg/kg body weight was administered orally to treat the breast cancer-bearing animals for consecutive 45 days. Interestingly, D-Pinitol significantly decreased the lipid peroxidation and increased the antioxidants and modulated the biotransformation enzymes to near normal level when compared to control. The western blotting and RT-PCR analysis also inevitably confirms that D-Pinitol treatment down regulated the expression of Bcl-2 and up regulated the p53 and caspase-3 proteins. The histological analysis of breast and liver tissues were well supported the protective role of D-Pinitol. Thus, the therapeutic property of D-Pinitol might be due to its strong antioxidant and remarkable induction in phase II and significant modulation in phase I drug metabolizing enzymes and prominent influence in the proteins of apoptotic, anti-apoptotic and tumor suppressors which ultimately end up with the consideration of D-Pinitol in the treatment of genotoxin mediated carcinogenesis.

The aim of the study was to evaluate the protective activity of D-Pinitol against carbon tetrachloride (CCl4)-induced hepatotoxicity in rats. The animals were divided into six groups, with each group consisting of six animals. Group I animals served as normal controls and received olive oil vehicle (1.0 ml/kg body weight intraperitoneally). Group II rats served as CCl4 controls, which received 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks. Group III rats were treated with 30% CCl4 suspended in olive oil (3.0 ml/kg body weight intraperitoneally) twice a week for 4 weeks, followed by D-Pinitol (100 mg/kg body weight) given for 28 days intragastrically. Group IV rats received D-Pinitol alone at a concentration of 100 mg/kg body weight for 28 days intragastrically. At the end of the experimental period, serum marker enzymes and lipid peroxidation (LPO) levels were significantly increased in group II animals. On the other hand, D-Pinitol treatment significantly decreased marker enzymes and LPO levels and increased the antioxidant level. CYP expression was also investigated. Therefore, the present study revealed that D-Pinitol acts as a protective agent by decreasing metabolic activation of xenobiotics through its antioxidant nature.

Hepatocellular carcinoma is one of the most common cancers and lethal diseases in the world. Recently, many researchers focused to identify novel chemotherapeutic agents from natural sources against hepatocarcinogenesis. The diverse therapeutic potential of essential oils has drawn the attention of researchers to test them for anticancer activity, taking advantage of the fact that their mechanism of action is dissimilar to that of chemotherapeutic agents. Earlier reports indicated that essential oil components, especially monoterpenes, have multiple pharmacological effects which could account for the terpene-tumor suppressive activity. In the present study, it is shown that myrtenal, a natural monoterpene, which acts as an antineoplastic agent against diethylnitrosamine induced phenobarbital promoted experimental hepatocellular carcinoma. The results revealed an elevated level of microsomal lipid peroxidation in the liver, which was found to be significantly reduced by myrtenal treatment. On the contrary, the Phase I hepatic drug metabolizing enzymes' (cytochrome P(450), cytochrome b(5), NADPH-cytochrome c reductase, NADH-cytochrome b(5) reductase) levels were decreased and the Phase II enzymes (glutathione-S-transferase, uridine 5'-diphospho-glucuronyl transferase) were increased in carcinogen-administered animals, which were reverted to near normalcy upon myrtenal administration. Our findings also showed that myrtenal restrains the liver cancer by preventing the DEN-PB induced up-regulation of TNF-α protein expression by immunoblot. Furthermore, transmission electron microscopic examination also indicated that myrtenal prevents the carcinogen-induced changes in the architecture of liver tissue and cell structure. Thus, this study shows that myrtenal has the ability to suppress the hepatocellular carcinoma in rats.

Traditionally, dietary compounds have been practiced to eliminate toxins and to strengthen the defense system towards resistance to many disease. d -Pinitol is one of a natural dietary compound predominantly found in soy products. It has been reported to possess diverse biological properties and their therapeutic properties propel them to evaluate against various experimental diseases. We have reported here the protective role of d -Pinitol on renal and hepatic tissue against oxidative stress mediated experimental breast cancer model. DMBA, the polycyclic aromatic hydrocarbon, was used to induce breast cancer in female Sprague Dawley rats with single oral dose of 20 mg/kg/body weight diluted in corn oil. The cancer-bearing rats were treated with the natural dietary compound d -Pinitol at the concentration of 200 mg/kg/body weight orally for 45 days. We observed that d -Pinitol significantly restored the elevated levels of marker enzymes such as ALT, AST and LDH and efficiently down regulates lipid per-oxidation and lysosomal enzymes. The antioxidants levels were found to be significantly enhanced and the carbohydrate key metabolizing enzymes were excellently modulated towards normal range. These biochemical alterations were well reflected in the histopathological studies of liver and kidney tissues of control and experimental groups. Thus, the hepatic and renal tissue protective property might be due to the antioxidant activity which might reduce the per-oxidation reaction that were induced by DMBA and also render protection to the membrane integrity through its firm antioxidant property and modulatory role with prominent intervention strategies in gluconeogenesis process and lysosomal enzymes.

Myrtenal, a natural monoterpene occurred in cumin, pepper, mint and eucalyptus. Monoterpenes are naturally occurring plant hydrocarbons composed of two isoprene units and are widely distributed in plant flora and are best known for occurrence in essential oils. Monoterpenes have been shown to have remarkable biological activities such as antioxidant, chemotherapeutic and chemopreventive effects in different models of cancer. The aim of the study was to investigate the antioxidant and anticancer activity of myrtenal against carcinogen induced hepatocellular caricinoma in rats.The antioxidant properties of myrtenal were evaluated by using different in vitro antioxidant assays such as by determining its scavenging effect against hydroxyl (OH(•)), superoxide anion (O2(•-)), nitric oxide, 1,1-diphenyl-2-picrylhydrazyl (DPPH(•)) and 2,2-azino-bis-3-ethylbenzothiazoline-6-sulphonic acid radical cation (ABTS(•+)). In vivo antioxidant and anticancer activity of myrtenal were evaluated by determining the antioxidant enzymes, apoptotic and anti-apoptotic proteins such as Bcl-2, Bax and caspase-3 expression and histopathological analysis against the diethylnitrosamine induced hepatocellular carcinoma in wistar albino rats.Our results demonstrated that myrtenal exhibits strong antioxidant property in all the in vitro assays and the in vivo results revealed that the antioxidant status was significantly decreased in hepatoma bearing animals. The expression of anti-apoptotic proteins was up regulated and in contrast the apoptotic protein was down regulated in hepatoma bearing animals. Treatment with myrtenal to cancer bearing animals resulted in remarkable increase in the inherent antioxidants and excellent modulation in the proteins of apoptotic and anti-apoptotic cascade. Further, the RT-PCR analysis of protein expressions and histological analysis of liver tissues inevitably confirms the anticancer property of myrtenal.It is concluded that myrtenal exhibits excellent free radical scavenging activity and anticancer activity through the suppression of hepatocellular carcinoma in wistar rats. Thereby giving a positive insight to take this compound as an effective therapeutic agent against hepatoma.

Compounds of dietary origin have always been considered as a paramount entity due to their popular belief of the absence of adverse side effects and also for their extraordinary efficacy against many diseases among which cancer is most important. The present investigation was aimed to evaluate the modulatory effect of d -Pinitol a compound from dietary origin, on the key mitochondrial tricarboxylic acid cycle, carbohydrate metabolizing enzymes and anti-apoptotic protein Bcl-2 against 7, 12-Dimethylbenz [a] anthracene (DMBA) induced mammary carcinoma in female Sprague Dawley rats. Breast caner was induced by intragastric administration of single dose of 20 mg/kg body weight of DMBA. The results revealed that the levels of TCA cycle enzymes and carbohydrate metabolizing enzymes were drastically altered in both breast and liver tissues of cancer-bearing animals when compared to controls. Further, the anti-apoptotic protein Bcl-2 was found to be expressed during breast cancer. Interestingly, the oral administration of d -Pinitol at a dosage of 200 mg/kg body weight for 45 days to breast cancer-bearing rats were found to be significantly brought back the altered enzymes status to near normal range. This therapeutic activity may be due to the antioxidant property of d -Pinitol, which ultimately results in the mitochondrial compartment. Thus, our results clearly confirmed that d -Pinitol has some key modulatory property in mitochondrial and carbohydrate metabolizing enzymes through its antioxidant nature and also regulatory role in the proteins of anti-apoptotic cascade against the free radicals involved oxidative stress-mediated diseases, and which results in the consideration of the compound as safe and more effective in the treatment of mammary carcinoma in the near future.

Objective The present study was aimed to scrutinize the anticancer consequence of kaempferol against aflatoxin B1 induced hepatocarcinogenesis. Epidemiological studies of the incidence of liver cancer in the population, where dietary aflatoxin exposure is high, have provided much circumstantial evidence for the development of aflatoxin B1 induced primary liver cancer in humans. Methods In the present investigation, aflatoxin B1 (2 mg/kg body weight i.p) was used as a hepatocarcinogen to induce hepatocellular carcinoma in experimental animals. Results In the present analysis, on treatment with bioflavonoid kaempferol (100 mg/kg body weight p.o) the nucleic acids levels were brought back to normal and also the altered levels of biological enzymes such as membrane bound ATPase, carbohydrate metabolizing enzymes and mitochondrial TCA cycle enzymes levels ( P Conclusions Membrane bound ATPase, carbohydrate metabolizing enzymes and mitochondrial TCA cycle enzymes were modulated by kaempferol evaluated on aflatoxin B1 induced primary liver carcinogenesis.

Hesperidin a natural flavanoglycoside, has demonstrated a wide variety of biological activities which make it a good candidate for the treatment of many oxidative stress mediated diseases. The present study was aimed to evaluate its therapeutic potential by assaying the activities of lipid peroxidation and various membrane bound marker enzymes in 7, 12-Dimethybenz (a) anthracene induced breast cancer rats. The daily oral treatment of hesperidin (30 mg/kg body weight) to breast cancer bearing rats for 45 days demonstrated a significant ( p p

The present study was aimed to investigate the therapeutic effect of hesperidin with reference to hepatic biotransformation, lysosomal and mitochondrial TCA cycle enzymes against 7,12-dimethylbenz(a)anthracene (DMBA)-induced experimental breast cancer. DMBA is a major class of chemical carcinogen present in the environment and it may increase breast cancer risk. In the present investigation, 7,12-DMBA was used as a carcinogen to induce breast cancer in rats. Hesperidin, a natural flavanoglycoside has demonstrated a wide variety of biological activities which make it a good candidate for the treatment of many oxidative stress-mediated diseases. In this study the hepatic biotransformation (Phase I, Phase II) enzymes were analyzed both in breast and liver. The lysosomal enzymes were analyzed in breast tissues and the key mitochondrial TCA cycle enzymes were analyzed in liver. The results revealed that treatment with hesperidin (30 mg/kg body weight) significantly restored all the altered biochemical parameters. The ultra structural analysis of breast and histology of liver tissues inevitably supports the biochemical alterations and this was attributed due to the interaction of flavonoid hesperidin through the induction or inhibition of metabolism and also the modulating property in the lysosomal and TCA cycle compartments.

The present study was designed to evaluate the nephroprotective role of methanolic extract of Achyranthes aspera (A.aspera) an important herb in the Indian system of medicine against lead acetate-induced nephrotoxicity in rats. Toxicity was induced in male albino rats (Wistar strain) by administering lead acetate (0.2%) in drinking water for 6 weeks, followed by extract of A. aspera (200 mg/kg body weight). Changes in kidney weights encountered upon lead administration improved after extract with A. aspera. Lead damage to the urine was evident from increase in the activity of γ-glutamyltranspeptidase (γ-GT), Cathespin D, alkaline phosphatase (ALP), acid phosphatase (ACP), β-glucuronidase lactate dehydrogenase (LDH) and N-acetyl-β-D-glucosaminidase (NAG) in urine along with some urinary constituents (urea, uric acid, creatinine, protein and phosphorous). The effects of lead were also studied in kidney (γ-GT, β-glucuronidase, NAG, Cathespin D and LDH) and showed a decline upon extract administration. Increased activities of urinary enzymes were accompanied by increase in the urinary constituents. Treatment with methanolic extract of A. aspera after lead induction completely ameliorated the lead-induced renal damage.

Perna viridis is an ideal animal for studying the impairment caused by the effects of heavy metals that are often detected in coastal areas. Preliminary bioassay tests revealed that the lethal (LC(100)), median lethal (LC(50)) and sublethal (LC(0)) concentration of silver and chromium to P. viridis were 6.5, 4.0, 2.0 mg l(-1) and 4.5, 2.5, 1.0 mg l(-1), respectively. Toxic effect of silver and chromium was evaluated in the green mussel P. viridis, with reference to oxygen consumption, filtration rate and ATPase system in laboratory experiments. These parameters were selected as the end point of sublethal stress. Oxygen consumption and filtration rates were calculated as a measure of decline in the dissolved oxygen level and algal concentration (feed) in the aquaria water, respectively. Silver and chromium affects both oxygen consumption and filtration rate significantly (P0.01) at 96 h when compared to control. The activity of ATPases system in the gills, hepatopancreas, ovary and muscle of mussels were inhibited by silver and chromium indicating that metals exerted significant toxic effect. The inhibition of Na(+)K(+) ATPase, Ca(2+) ATPase and Mg(2+) ATPase in the mussels were significant (P0.05) for silver and highly significant (P0.01) for chromium, which indicates that chromium was more toxic to mussels when compared to silver. The assessment of oxygen consumption, filtration and ATPases system can thus be used as a valid biomarker in aquatic ecotoxicology studies.

Alcoholic extract of the marine algae Chlorella vulgaris was examined for its free radical scavenging effect with reference to naphthalene-induced lipid peroxidation in serum, liver, and kidney of rats. Initially, upon naphthalene intoxication (435 mg/kg body weight, intraperitoneally), the lipid peroxidation activity increased significantly (P < 0.001), and in contrast, the enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymic antioxidants (glutathione, ascorbic acid, and α-tocopherol) levels decreased remarkably. When the naphthalene stressed rats were treated with Chlorella vulgaris extract (70 mg/kg body weight, orally), the lipid peroxidation activity reduced significantly (P < 0.001) and the activities of both the enzymic and non-enzymic antioxidants increased reaching near control values. The minimum concentration (70 mg/l) of the extract that exhibited maximum (85%) free radical scavenging activity was chosen for the experimental study. The present results suggest that Chlorella vulgaris extract exerts its chemo-preventive effect by modulating the antioxidants status and lipid peroxidation during naphthalene intoxication.

The sublethal effect of silver and chromium on some biochemical constituents was studied in the green mussel Perna viridis. The results revealed an overall reduction in total protein, total DNA, total RNA, glycogen, protein bound sugars and total lipid in the gill, hepatopancreas, and ovary of the mussels exposed to metals individually and in combination when compared with control. It was apparent that mussels exposed to mixtures of metals exhibited highly significant (P

The protective effects of vitamins C and E against oxidative stress were evaluated in various tissues of thornfish Terapon jarbua exposed to copper. Preliminary bioassay tests performed with copper and T. jarbua revealed that 4.0, 2.5 and 1.0 mg L(-1) of copper were lethal (LC(100)), medial lethal (LC(50)) and sublethal (LC(0)) respectively. Oxidative stress parameters viz. lipid peroxidation, superoxide dismutase, catalase, glutathione peroxidase, and glutathione were evaluated in control and experimental fishes. Lipid peroxidation activity increased in tissues of copper exposed fishes, while the antioxidant system exhibited a reduction in their activity. On the contrary copper stressed fishes fed with vitamins C and E enriched pellet feed showed significant reduction in lipid peroxidation activity and the antioxidant levels increased reaching near normal levels comparable to control values. Bioaccumulation of copper was studied in addition to oxidative stress. Substantial copper residue was detected in the tissues of T. jarbua exposed to copper and the level of copper in tissues reduced when the fishes were treated with vitamins ensuring copper depuration and thereby protecting them against stress. We concluded that vitamin supplementation offered significant reduction of the oxidative stress mediated by copper and we discuss the possible application of vitamins in costal aquaculture process.

The sublethal effect of naphthalene was studied on the physiology of a mud crab Scylla serrata. The 96 h acute toxicity of naphthalene was determined and found to be 28 mg 1(-1) (LC100), 18 mg 1(-1) (LC50), 10 mg 1(-1) (LC0) respectively. The 30 days sublethal effect (LC0) 9 mg 1(-1), 8 mg 1(-1), 10 mg 1(-1), of naphthalene was investigated in the crab S. serrata with reference to oxygen consumption and changes in the activity of respiratory enzymes. The results indicated that naphthalene caused disturbance in the normal physiology of the crab. The bioaccumulation of naphthalene was also investigated in gills, hepatopancreas, haemolymph and ovary. The consumption of oxygen increased in the naphthalene medium when compared with that of the crabs exposed to naphthalene free medium. A decreased trend in the activity of respiratory enzymes such as lactate dehydrogenase (LDH), isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), alpha-ketoglutarate dehydrogenase (alpha-KDH) and glutathione (GSH) were recorded in the hepatopancreas, ovary and gills of S. serrata for all the tested concentrations of naphthalene and the results were analyzed for their significance.

Epidemiological investigations have shown that overcoming the risk of cancer is related to the consumption of green vegetables and fruits. Many compounds from different origins, such as terrestrial plants and marine and microbial sources, have been reported to have therapeutic effects of which marine sources are the most important because the diversity of marine life is more varied than other sources. Fucoxanthin is one important compound with a marine origin and belongs to the group of carotenoids; it can be found in marine brown seaweeds, macroalgae, and diatoms, all of which have remarkable biological properties. Numerous studies have shown that fucoxanthin has considerable medicinal potential and promising applications in human health. In this review, we summarize the anticancer effects of fucoxanthin through several different mechanisms including anti-proliferation, induction of apoptosis, cell cycle arrest and anti-angiogenesis, and its possible role in the treatment of cancer.

Diosgenin, a natural steroidal saponin, has been reported to be found predominantly in fenugreek and has diverse biological properties. N-Methyl-N-nitrosourea (NMU) is a mammary gland-specific carcinogen that closely mimics human breast cancer in many aspects. The aim of this study was to investigate the anticarcinogenic property of diosgenin with reference to lipid peroxidation, status of antioxidants, and activities of marker enzymes against NMU-induced experimental mammary carcinogenesis. Breast cancer was induced in female Sprague Dawley rats by an intraperitoneal administration of a single dose of NMU (a concentration of 50 mg/kg body weight) diluted in 0.9% saline, and the rats were treated with oral diosgenin, 20 mg/kg body weight, for 45 days. The results were interesting, and the diosgenin treatment remarkably downregulated the peroxidation reaction and marker enzymes and extraordinarily enhanced the indigenous antioxidant defense system. The factor for this remarkable restoration might be due to the effect of the intervention strategy on the downregulation of the peroxidation reaction through the strong antioxidant nature, which ultimately reflected in the downregulation of marker enzyme activities. The histopathological study of breast and liver tissues inevitably confirms the biochemical changes. Thus, it can be concluded that diosgenin exhibits anticarcinogenic activity via reducing peroxidation reaction and marker enzymes through enhancing the intrinsic antioxidant defense system.

To find out the anticancer effect of Indigofera aspalathoides (I. aspalathoides) on 20-methylcholanthrene induced fibrosarcoma in rats.Fibrosarcoma was induced in Wistar strain male albino rats by 20-methylcholanthrene. Intraperitoneous (i.p.) administration of 250 mg/kg body weight/day of aqueous extract of I. aspalathoides for 30 d effectively suppressed chemically induced tumors. Parameters such as body weight, liver and kidney weight, tumor weight, mean survival time, behavioral changes, blood glucose, blood glycogen and marker enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), acid phosphatase (ACP) and 5'-nucleiotidase (5'-NT) in serum, liver and kidney and lipid profiles such as total cholesterol, phospholipids, free fatty acids in liver and kidney of control and experimental animals were studied.Fibrosarcoma bearing animals were ferocious and anxious. The mean survival time was found to increase after the treatment. The body weights were significantly decreased (P0.001) in group II fibrosarcoma animals which steadily increased after the treatment with I. aspalathoides. The liver and kidney weights were significantly increased whereas the tumor weights decreased as compared to the weights in untreated fibrosarcoma bearing rats. The blood glucose and the liver and kidney glycogen levels were found to decrease significantly (P0.001) in group II animals. Elevated activities of marker enzymes were observed in serum, liver and kidney of fibrosarcoma bearing Group II animals which were normalize after I. aspalathoides treatment. In the liver and kidney of Group II animals the total cholesterol increased whereas the phospholipids and free fatty acid levels decreased (P0.001) which were normalized after treatment.The treatment by I. aspalathoides on fibrosarcoma bearing rats has improved the levels of various parameters indicating its antiproliferative and anticancer activity.

We have reported here that the ameliorative potentials of D-Pinitol during 7, 12-Dimethylbenz [a] anthracene induced experimental breast carcinogenesis. DMBA is a potent organ specific carcinogen which is widely employed to induce mammary carcinoma in rats. D-Pinitol a natural inositol has been reported to found in soybean with many biological functions. The female sprague dawley rats were subjected to carcinogen 7, 12-DMBA and the ameliorative potentials of dietary compound D-Pinitol was investigated with reference to cell surface glycoproteins, lysosomal enzymes and adenosine triphosphatases. Interestingly, administration of D-Pinitol was found to be significantly down regulated the breast tissue glycoproteins and lysosomal enzymes and in contrast the levels of adenosine triphosphatases were remarkably up regulated. Further, the biochemical changes were well reflected and evidenced in the histology of breast and liver tissues. Thus, it can be concluded from the present study that D-Pinitol efficiently attenuates the hazardous consequences of the environmental carcinogen 7,12-DMBA through modulating cell surface glycoproteins, membrane protective role both in lysosomal and ATPase compartment via its antioxidant nature which ultimately results in the findings of future innovative remedies for genotoxin mediated hazards.

DMBA is a major class of potent genotoxic chemical carcinogen present in the environment and it may increase breast cancer risk. Flavonoids have been shown to have interesting biological activities in many experimental investigations. Hesperidin is one of the citrus flavonoid shown to be active against various oxidative stress mediated diseases. The aim of the present study was to investigate the beneficial impact of a natural citrus flavonoglycoside hesperidin against 7, 12-Dimethylbenz [a] anthracene challenged experimental breast carcinogenesis with reference to drug metabolizing enzymes and intrinsic antioxidant status. The female Sprague-Dawley rats were orally administered with single dose of 7, 12-DMBA to induce breast cancer and were treated with hesperidin [30mg/kg/body weight] for a consecutive 45 days. The results revealed that there was a significant reduction in the status of antioxidants levels and also significant alterations in the drug metabolizing enzymes were found in genotoxin DMBA exposed animals. Interestingly these, altered levels were significantly revered back to near normal in hesperidin administered animals via enhancing the intrinsic antioxidant levels and induction in Phase II enzymes and modulation in Phase I enzyme levels. Thus the antigenotoxic activity of hesperidin may be due to the modulatory effect in biotransformation enzymes and excellent antioxidant potentials which paving a way to consider hesperidin against the genotoxin involved oxidative stress mediated diseases.

Therapeutic substances may reduce the risk of developing cancer by modulating the factors responsible for carcinogenesis. To evaluate these hypotheses, the present study was designed to investigate the modulatory effect of bioflavonoid "Hesperidin" against DMBA induced experimental breast cancer with reference to renal cell surface glycoproteins, nucleic acids, protein content, lipid profile and lysosomal enzymes. The female sprague-dawley rats were orally administered with single dose of 7, 12-DMBA to induce breast cancer and were treated with hesperidin [30 mg/kg/body weight] for a consecutive 45 days. The results revealed that there was a significant elevation in the levels of glycoproteins, nucleic acids, lysosomal enzymes and also significant alterations in macromolecules in renal tissues of cancer bearing animals. Interestingly, the altered levels of these parameters were remarkably reverted back to near normal in hesperidin treatment. The histopathological analysis of liver and kidney tissues were well supported the biochemical alterations and inevitably proves the protective role of hesperidin. It is proposed that, the effect of hesperidin during DMBA induced breast cancer could be due to the intervention strategies of hesperidin in the protein, nucleic acid biosynthesis, membrane stabilizing potentials on lysosomal compartment and inhibitory effect on cell surface glycoproteins and bio-fuel such as lipids.

The present study was undertaken to test the chemopreventive effects of one herbal medicinal plant,Indigofera aspalathoides, on chemically induced carcinogenesis in rats. A well-known polyaromatic hydrocarbon, namely, 20-methylcholanthrene, which is a known carcinogenic substance, was used to induce fibrosarcoma in Wistar strain of male albino rats. Fibrosarcoma rats were treated with aqueous extracts ofIndigofera aspalathoides. The rats were divided into four groups, each consisting of six animals. Group I served as normal control, Group II served as fibrosarcoma-induced animals, Group III were fibrosarcoma-bearing animals treated with aqueous extracts ofIndigofera aspalathoides, and Group IV animals, which were normal healthy animals treated withIndigofera aspalathoidesaqueous extract, served as drug control set. Group III and Group IV animals were treated with aqueous extract ofIndigofera aspalathoidesintraperitoneally at a dose of 250 mg/kg. b.w. for 30 days. The fibrosarcoma was proved by pathological examinations. The activity levels of nucleic acids such as total DNA and RNA and hexose, hexosamine, and sialic acid in liver and kidney of treated rats were used to monitor the chemopreventive role of the plant extract. The observed increase in the levels of DNA, RNA, hexose, hexosamine, and sialic acid in liver and kidney tissues of fibrosarcoma-bearing animals reached near normal state after the treatment with aqueous extracts ofIndigofera aspalathoides, suggesting thatIndigofera aspalathoidesdoes have a chemotherapeutic role.

Hesperidin has been reported to have an excellent and wide variety of biological activities. This property has brought the compound to a new stage in the treatment of various oxidative stress-mediated diseases. The present investigation was aimed to evaluate the therapeutic potential of hesperidin by assaying the activities of antioxidant enzymes, lipid peroxidation, membrane bound marker enzymes, adenosine triphosphates, and TCA cycle enzymes, especially in kidney tissues during 7,12-dimethybenz(a)anthracene-induced breast cancer. Daily oral administration of hesperidin (30 mg/kg body wt) to breast cancer-bearing rats for 45 days demonstrated a significant (P < .05) decline in renal lipid peroxidation and membrane bound marker enzymes, as well as a remarkable increase in adenosine triphosphatases, mitochondrial functional enzymes, and renal antioxidants. Furthermore, histological studies of liver and kidney provided evidence of biochemical alterations. Thus, the protective effects of hesperidin on attenuating the peroxidation reaction and membrane bound marker enzyme activities as well as upregulation of adenosine triphosphatases, TCA cycle enzymes, and antioxidants suggest promising uses of flavonoglycoside hesperidin in the future treatment of oxidative stress-mediated diseases.

Background: The anticancer and antioxidant effects of the aqueous extract of Indigofera aspalathoides on 20-methylcholanthrene (20-MCA) induced fibrosarcoma were investigated in male albino rats. Materials and Methods: The rats were divided into four different groups, each group consisting of six animals. Group I animals were served as normal control, Group II animals were fibrosarcoma-bearing animals after the incubation period, Group III animals were fibrosarcoma-bearing animals, treated with aqueous extract of I. aspalathoides intraperitoneally at a dose of 250 mg/kg b.w. for 30 days and Group IV animals were administered with the aqueous extract of I. aspalathoides alone, at a dose of 250 mg/kg b.w. for 30 days, served as drug control animals. After the experimental period, all the rats were weighed and killed by cervical decapitation. The serum was separated from the blood for analysis. The weights of the liver and the kidneys were noted. The fibrosarcoma was proved by pathological examinations. The liver and kidney tissues were excised and then homogenized in an ice-cold buffer. These tissues were used for biochemical analysis. Results: The activities of antioxidant enzymes, e.g. catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), in blood serum, liver, and kidney of control and experimental animals, respectively, have been reported. Conclusion: The present observations suggested that the aqueous extract of I. aspalathoides treatment enhanced the recovery from 20-MCA-induced fibrosarcoma due to its antioxidants and antineoplastic properties.

In this paper, we present the stability analysis of delay differential equations which arise as a result of transportation lag in the CSTR‐mechanical separator recycle system. A first order irreversible elementary reaction is considered to model the system and is governed by the delay differential equations. The DDE‐BIFTOOL software package is used to analyze the stability of the delay system. The present analysis reveals that the system exhibits delay independent stability for isothermal operation of the CSTR. In the absence of delay, the system is dynamically unstable for non‐isothermal operation of the CSTR, and as a result of delay, the system exhibits delay dependent stability.

Biomarkers are useful tools for understanding complex interactions that elicit organisms response to environmental pollutants and their sublethal effects on organisms health. Effect of naphthalene on vitellogenin (VTG) and vitellin (VTN) were assessed in hepatopancreas, haemolymph and ovary of an estuarine crab Scylla serrata with reference to vitellogenic phases. In addition, the gonadosomatic index (GSI) was also assessed. Significant reductions in VTG and VTN contents were observed in hepatopancreas, haemolymph (VTG) and ovary (VTN). The GSI exhibited a decreasing trend in crabs exposed to naphthalene irrespective of the vitellogenic phases. We attempted to use the alterations in vitellogenic proteins and GSI as biomarkers of reproductive disturbances occurred in the crab due to naphthalene stress.

AIM: To investigate the effects of Terminalia arjuna (T. arjuna) extract on human hepatoma cell line (HepG2) and its possible role in induction of apoptosis. METHODS: Human hepatoma cells were treated with different concentrations of ethanolic extract of T. arjuna and its cytotoxicity effect was measured by trypan blue exclusion method and lactate dehydrogenase leakage assay. Apoptosis was analyzed by light and fluorescence microscopic methods, and DNA fragmentation. The mechanism of apoptosis was studied with expression of p53 and caspase-3 proteins. Glutathione (GSH) content was also measured in HepG2 cells after T. arjuna treatment. RESULTS: T. arjuna inhibited the proliferation of HepG2 cells in a concentration-dependent manner. Apoptotic morphology was observed in HepG2 cells treated with T. arjuna at the concentrations of 60 and 100 mg/L. DNA fragmentation, accumulation of p53 and cleavage of procaspase-3 protein were observed in HepG2 cells after the treatment with T. arjuna. The depletion of GSH was observed in HepG2 cells treated with T. arjuna. CONCLUSION: T. arjuna induced cytotoxicity in HepG2 cells in vitro. Apoptosis of HepG2 cells may be due to the DNA damage and expression of apoptotic proteins. Depletion of GSH may be involved in the induction of apoptosis of HepG2 cells.

The present investigation was carried out to evaluate the antioxidant nature of ethanolic extract of Terminalia arjuna bark (EETA) on N-nitrosodiethylamine (DEN) induced liver cancer in male Wistar albino rats. Liver cancer was induced by single intraperitonial injection of DEN (200 mg/kg). After 2 weeks of DEN administration, Phenobarbital (PB) was given to promote the cancer for up to 14 successive weeks. EETA extract (400 mg/kg) was given post-orally for 28 days to hepatocellular carcinoma-bearing rats. After the experimental period, all the animals were sacrificed and serum, liver and kidney samples were collected for further biochemical analysis. The levels of lipid peroxides (LPO) under basal and also in the presence of inducers (H(2)O(2), ascorbate and FeSO(4)) were estimated in serum, liver and kidney of control and experimental animals. Enzymic antioxidants, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and non-enzymic antioxidants like Vitamin C (Vit-C) and Vitamin E (Vit-E) levels were determined in all the groups of animals. A significant increase in LPO levels were observed while the levels of enzymic and non-enzymic antioxidants were decreased, when subjected to DEN induction. These altered enzyme levels were ameliorated significantly by administration of EETA at the concentration of 400 mg/kg in drug-treated animals. This protective effect of EETA was associated with inhibition of LPO induced by DEN and to maintain the antioxidant enzyme levels. Our results show an antioxidant activity of T. arjuna bark against DEN-induced liver cancer.