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Quercetin (3,5,7,3',4'-pentahydroxy flavone) is a potent antioxidant found in various fruits and vegetables. The present investigation was an attempt to evaluate the mitigatory effect of quercetin on the damage caused by bisphenol A (BPA; 2,2-bis (4-hydroxyphenyl) propane), a well-known xenoestrogen, on liver and kidney of mice. Swiss strain adult male albino mice were orally administered with 120 and 240 mg/kg body weight (bw)/day BPA with or without quercetin (60 mg/kg bw/day) for 30 days. On the completion of the treatment period, animals were killed; organs were isolated and used for the study. Results revealed that oral administration of BPA for 30 days caused significant and dose-dependent decrease in body weight. Absolute and relative organ weights, total lipid and cholesterol contents were significantly increased in liver and kidney of mice when compared with vehicle control. BPA treatment also caused, when compared with vehicle control, a statistically significant reductions in the activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as in glutathione and total ascorbic acid contents; however, significant increase was found in malondialdehyde (MDA) levels. Histopathological studies revealed hepatocellular necrosis, cytoplasmic vacuolization and decrease in hepatocellular compactness in liver as well as distortion of the tubules, increased vacuolization, necrosis and disorganization of glomerulus in the kidney of BPA-treated mice. All these effects were dose-dependent. Co-treatment with quercetin (60 mg/kg bw) and BPA (low dose and high dose) alleviates the changes in body weight, as well as absolute and relative organ weights of mice. It also ameliorates the oxidative stress created by BPA by lowering MDA levels and by increasing enzymatic and nonenzymatic antioxidants as well as it brings back the normal histoarchitecture of liver and kidney of mice. The present results revealed that graded doses of BPA caused oxidative damage in liver and kidney of mice, which is mitigated by quercetin., (© The Author(s) 2012.)

This article describes antioxidative and cytoprotective property of andrographolide, a major active component of the plant Andrographis paniculata (A. paniculata). High yields (2.7%) of andrographolide was isolated from the aerial parts of this plant via silica column chromatography. The purity of the compound was determined by high-performance thin-layer chromatography (HPTLC) and reversed phase high-performance liquid chromatography (HPLC) analysis. The structure was elucidated using techniques such as UV-visible spectrophotometry, elemental analysis, Fourier transform infrared (FT-IR), (1)H nuclear magnetic resonance ((1)H NMR), (13)C nuclear magnetic resonance ((13)C NMR) and mass spectral analysis and the data obtained were comparable with reported results. It was observed that andrographolide exhibited significant antioxidative property (IC50 = 3.2 µg/ml) by its ability to scavenge a stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) as compared to known antioxidants like ascorbic acid, butylated hydroxy toluene (BHT) and the plant extract. The cytoprotective role of andrographolide against carbon tetrachloride (CCl4) toxicity in human hepatoma HepG2 cell line was assessed using trypan blue exclusion test, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, by estimation of various leakage enzymes and by measuring the glutathione levels. The recovery obtained for andrographolide treatment in the presence of CCl4 was two-fold compared to A. paniculata extract for all other related biochemical parameters investigated. The results of the study indicate that andrographolide is a potent inhibitor of CCl4-mediated lipid peroxidation.

Prime focus of the present investigation was to evaluate hepatoprotective potency of Ocimum sanctum (O. sanctum) aqueous extract against butyl p-hydroxybenzoic acid (butylparaben) toxicity in mice. Oral treatment of butylparaben (1320 mg/kg b.w./day) to mice for 30 days resulted in significant (p < 0.05) elevation in hepatic lipid peroxidation, which could be due to significant (p < 0.05) reduction in non-enzymatic (glutathione and total ascorbic acid) antioxidant contents and enzymatic (superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione transferase) antioxidants activities. Co-treatment of O. sanctum extracts in three different doses (100, 200 and 300 mg/kg b.w./day) resulted in significant (p < 0.05) reduction in butylparaben-induced hepatic changes. Oral administration of O. sanctum with butylparaben resulted in dose-dependent and significant (p < 0.05) reduction in lipid peroxidation as compared to butylparaben alone treated group. Similarly, all three doses of O. sanctum reduced butylparaben-induced changes in non-enzymatic and enzymatic antioxidants. The effect was significant (p < 0.05) and dose-dependent. All three doses of O. sanctum ameliorated butylparaben-induced changes, showing maximum protection at 300 mg/kg b.w./day dose. Results of present study indicate that butylparaben-induced hepatotoxicity involves its ability to induce oxidative stress, whereas antihepatotoxic effect of O. sanctum was mainly due to its antioxidative potency.

Aflatoxin belongs to the class of naturally occurring mycotoxins, food contaminants having potent carcinogenicity. We have evaluated the ameliorative role of black tea extract on aflatoxin-induced biochemical changes in the liver of albino male mice. Adult male mice were orally administered with 750 and 1500 pg of aflatoxin in 0.2 mL olive oil/kg b.w./day for 30 days. Oral administration of aflatoxin caused, as compared with controls, significant, dose-dependent reduction in DNA, RNA, protein and glycogen contents; however, cholesterol content and phsphorylase activity were significantly increased. Black tea is one of the most potent antioxidants containing numerous bioactive phytonurtients having therapeutic applications. Aflatoxin-induced changes in the liver of mice were significantly ameliorated on co-treatment of black tea extract (2% infusion in water).

Present study focuses on the evaluation of butyl p-hydroxybenzoic acid (butylparaben CAS No: 94-26-8) exerted hepatotoxicity in mice. Oral administration of three different doses of butylparaben (40, 20 and 13.33 mg/0.2 mL olive oil/kg b.w./day) for 30 days has resulted in marked increase in lipid peroxidation. The effect was dose-dependent. Biochemical analysis revealed significant (p < 0.05) and dose-dependant reduction in non-enzymatic antioxidants such as glutathione and ascorbic acid content. Significant (p < 0.05) reduction in enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase were also observed in butylparaben treated groups as compared to control. Our findings prove that the oxidative stress induced by butylparaben plays the central role in the toxicity.

Liver disease has become a global concern worldwide. In absence of reliable liver protective drugs in modem medicine, a large number of medicinal preparations are recommended for the treatment of liver disorders as they are believed to be harmless based on their natural origin. The aim of the present study was to determine the hepatoprotective activity of Phyllanthus amarus plant extract against carbon tetrachloride (CCl4-induced liver damage in female mice. Carbon tetrachloride administration caused a significant increase in liver and serum alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP) and acid phosphatase (ACP), while total protein content significantly decreased as compared to vehicle control. The effect was dose-dependent. Oral administration of aqueous extract of Phyllanthus amarus along with carbon tetrachloride caused significant mitigation of CCl4-induced changes.

We have evaluated the ameliorative effect of ginger extract on paraben (p-hydroxybenzoic acid)-induced lipid peroxidation in the liver of mice. Adult female albino mice were orally administered with 2.25 or 4.50 mg of paraben in 0.2 mL olive/animal/day (67.5 and 135 mg/kg of body weight) for 30 days. The results revealed significantly higher (p < or = 0.05) lipid peroxidation in the liver of paraben-treated mice than that of controls. As compared with the controls, the levels of non-enzymatic antioxidants: glutathione and ascorbic acid, as well as the enzymatic antioxidants: superoxide dismutase, glutathione peroxidase and catalase were significantly (p < or = 0.05) lowered in the liver of paraben-treated mice. Oral administration of aqueous extract of Zinziber officinale (3 mg/animal/day) along with paraben for 30 days (Groups 6 and 7) caused significant (p < or = 0.05) amelioration in paraben-induced lipid peroxidation and increased significantly (p < or = 0.05) the activities of enzymatic (superoxide dismutase, glutathione peroxidase, catalase) and contents of non-enzymatic (glutathione and ascorbic acid) antioxidants in the liver of mice, as compared with those given paraben alone (Groups 4, 5). Thus, oral administration of aqueous extract of Zinziber officinale along with paraben significantly (p < or = 0.05) ameliorates paraben-induced lipid peroxidation in the liver of mice.

The aim of present study is to investigate the ameliorative effect of black tea extract on gasoline and GM-10 induced toxicity in liver of mice. Eighty healthy male mice weighing 38-40 g approximately were divided into eight groups which included untreated control and various treated groups. Mice were treated with Gasoline 462 mg/kg/day and GM-10 low dose (206 mg/kg/day) and high dose (412 mg/kg/day) subcutaneously for 30 days. Black tea extract was given as 2 g/100 mL drinking water (2% w/v) instead of pure drinking water. All the animals were sacrificed on 31st day by cervical dislocation and livers were isolated and weighed. Parameters such as lipid peroxidation, catalase, superoxide dismutase, glutathione peroxidase, glutathione and total ascorbic acid were studied. The results revealed dose-dependent toxicity of gasoline and GM-10 on liver. Administration of black tea extract ameliorates this toxicity of gasoline and GM-10 in liver of mice. This proves the effective ameliorative effect of black tea extract.

The present investigation was an attempt to evaluate the ameliorative effect of curcumin on aflatoxin-induced changes in activities of succinate dehydrogenase (SDH) and adenosine triphosphatase (ATPase) in liver and kidney of mice. Aflatoxin was obtained by growing Aspergillus parasiticus in SMKY liquid medium. Pure curcumin (97% purity) was purchased from Hi-Media Laboratories Pvt. Ltd., Mumbai, India. Young adult male albino mice were orally administered with low dose and high dose (750 and 1500 microg/kg body weight) aflatoxin with and without curcumin (2 mg/0.2 mLolive oil/animal/day) for 45 days. On 46th day the animals were sacrificed by cervical dislocation and organs were removed to prepare homogenates for measuring changes in enzyme activities such as succinate dehydrogenase and adenosine triphosphatase. The results showed that in liver and kidney of mice activities of both the enzymes succinate dehydrogenase and adenosine triphosphatase were found to be reduced in the groups treated with low dose and high dose of aflatoxin, which were ameliorated by the treatment of curcumin along with aflatoxin in other groups. Thus, curcumin along with aflatoxin ameliorates aflatoxin-induced changes in succinate dehydrogenase and adenosine triphosphatase activities in liver and kidney of mice.

The present investigation was an attempt to evaluate the ameliorative effect of curcumin on aflatoxin-induced lipid peroxidation in liver and kidney of mice. Aflatoxin was obtained by growing Aspergillus parasiticus in SMKY liquid medium. Pure curcumin (97% purity) was purchased from Hi-Media Laboratories Pvt. Ltd., Mumbai, India. Young adult male albino mice were orally administered with low dose and high dose (750 and 1500 microg/kg body weight) with and without curcumin (2 mg/0.2 mL olive oil/animal/day) for 45 days. On 46th day the animals were sacrificed by cervical dislocation. Liver and kidney were removed and weighed. Homogenates were prepared for measuring lipid-peroxidation along with changes in catalase, superoixide dismutase, glutathione, glutathione-peroxidase and total ascorbic acid. The results revealed concentration dependent increase in lipid peroxidation along with reduction in enzymatic and non-enzymatic antioxidants. Treatment with curcumin along with aflatoxin ameliorates aflatoxin-induced lipid peroxidation in liver and kidney of mice by ameliorating both enzymatic and non-enzymatic antioxidants.

The present investigation is an attempt to evaluate the ameliorative effect of curcumin on aflatoxin-induced toxicity in liver and kidney of mice. Aflatoxin was obtained by growing Aspergillus parasiticus in SMKY liquid medium. 70 male mice were divided into 7 groups (37-40 g body weight) including untreated control, vehicle control (0.2 mL olive oil/animal/day), curcumin control (50 mg/kg body weight/animal), aflatoxin low dose and high dose (750 and 1500 mg/kg body weight). Other two groups were administered curcumin along with low dose aflatoxin and high dose aflatoxin. The treatment was given for 45 days. On 46th day the animals were sacrificed by cervical dislocation. Liver and kidney were removed and weighed. Homogenates were prepared and analyzed for DNA, RNA and protein content. The results revealed dose-dependent significant reduction in DNA, RNA and protein contents in the liver and kidney of mice. Oral administration of aflatoxin along with curcumin significantly ameliorates, as compared to aflatoxin alone treated groups, in all parameters. It is concluded that curcumin ameliorates aflatoxin-induced toxicity in liver and kidney of mice.

The present investigation was an attempt to evaluate the possible ameliorative effect of curcumin on aflatoxin-induced lipid peroxidation in liver, kidney and testis of mice in vitro. Tissues were collected from healthy Swiss strain male albino mice Mus musculus weighing 30-35 g. The homogenates were treated with aflatoxin (2-10 mg/mL) with and without curcumin (25-200 mg/mL). The results revealed that addition of aflatoxin (2-10 mg/mL) to homogenates caused significant increase in lipid-peroxidation which was maximal at 6 mg/mL aflatoxin concentration. However, concurrent addition of aflatoxin (6 mg/mL) and curcumin ((25-200 mg/mL) caused concentration-dependent amelioration in aflatoxin-induced lipid peroxidation.

The present investigation was undertaken to evaluate the effect of paraben (p-hydroxybenzoic acid) on acidic, basic, and neutral proteins content, as well as carbohydrate and cholesterol contents in liver and kidney of mice. Adult female albino mice were orally administrated with 2.25 and 4.5 mg of paraben in 0.2 mL of olive/animal/day for thirty days. The results revealed dose dependent, significant reduction in acidic, basic, and neutral protein, carbohydrate contents and an increase in cholesterol content of the investigated liver and kidney. Oral administration of aqueous extract of Zinziber officinale (3 mg/animal/day) along with paraben for thirty days caused significant amelioration in all the protein types, carbohydrate and cholesterol of liver and kidney.

We have evaluated the ameliorative effect of black tea extract on aflatoxin-induced lipid peroxidation in the liver of mice. Adult male albino mice were orally administered with 25 and 50 microg of aflatoxin in 0.2 ml olive oil/animal/day for 30 days. Results revealed dose-dependent and significantly (p<0.05) higher lipid peroxidation in the liver of aflatoxin-treated mice than that of vehicle control. As compared with vehicle control, the levels of non-enzymatic antioxidants such as glutathione and ascorbic acid, as well as the enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase and catalase were significantly (p<0.05) lowered in the liver of aflatoxin-treated mice. Oral administration of two percent aqueous black tea extract along with aflatoxin for 30 days (groups 6 and 7) caused significant (p<0.05) amelioration in aflatoxin-induced lipid peroxidation by increasing significantly (p<0.05) the activities of enzymatic (superoxide dismutase, glutathione peroxidase, catalase) and contents of non-enzymatic (glutathione and ascorbic acid) antioxidants in the liver of mice as compared with those given aflatoxin alone (groups 4 and 5). Thus, oral administration of black tea along with aflatoxin significantly (p<0.05) ameliorates aflatoxin-induced lipid peroxidation in the liver of mice.

Oral administration of arsenic trioxide (3 and 6 mg/kg body weight/d) for 30 d caused, as compared with vehicle control, dose-dependent significant reductions in body weight, absolute weight, protein, glycogen, as well as, total, dehydro and reduced ascorbic acid contents both in the liver and kidney of arsenic-treated mice. Succinic dehydrogenase (SDH) and phosphorylase only in the liver activities were significantly reduced in a dose-dependent manner. Acid phosphatase activity was significantly decreased in the liver of low dose arsenic-treated animals; however, significant rise in its activity was observed in high dose group. As compared with vehicle control, treatment also caused significant dose-dependent reductions in SDH, alkaline phosphatase and acid phosphatase activities in the kidney of mice. Vitamin E cotreatment as well as, 30 d withdrawal of arsenic trioxide treatment with or without vitamin E caused significant amelioration in arsenic-induced toxicity in mice. Administration of vitamin E during withdrawal of treatment also caused significant amelioration as compared from only withdrawal of the treatment. It is concluded that vitamin E ameliorates arsenic-induced toxicities in the liver and kidney of mice.