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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).

Objective: To investigate the effect of curcumin on aflatoxin-induced biochemical changes in testis of mice., Design: Controlled research laboratory study., Setting: 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., Patient(s): Young inbred, Swiss strain male albino mice (Mus musculus), weighing approximately 37-40 g, were obtained from Cadila Health Care, Ahmedabad, India., Intervention(s): Aflatoxin was administered orally at 25 microg (low dose) and 50 microg (high dose)/0.2 mL olive oil/animal/day (750 and 1,500 microg/kg body weight), respectively, with and without curcumin for 45 days. On the 46th day the animals were sacrificed by cervical dislocation. Testis were removed and weighed. Homogenates were prepared for respective parameters such as protein, cholesterol, DNA, RNA, and 3beta- and 17beta-hydroxysteroid dehydrogenase activity., Main Outcome Measure(s): Protein, cholesterol, DNA, RNA, 3beta- and 17beta-hydroxysteroid dehydrogenase activity were measured immediately., Result(s): There was a dose-dependent effect of aflatoxin on testis of mice. Protein, cholesterol, DNA, RNA, and 3beta- and 17beta-hydroxysteroid dehydrogenase activity were reduced significantly by the treatment of aflatoxin; cholesterol was increased. Treatment with curcumin along with aflatoxin ameliorates aflatoxin-induced biochemical changes in the testis of mice., Conclusion(s): Curcumin significantly ameliorates aflatoxin-induced biochemical changes in the testis of mice.

Objective: To investigate the ameliorative effect of curcumin on aflatoxin-induced toxicity in mice spermatozoa., Design: Prospective controlled animal study., Setting: University research laboratory., Patient(s): Young, inbred, Swiss-strain male albino mice (Mus musculus), weighing approximately 37 to 40 g, were obtained from Cadila Health Care, Ahmedabad, India., Intervention(s): Aflatoxin was orally administered in 25 (low dose) and 50 (high dose) microg/0.2 mL olive oil to each animal, each day (750 and 1500 microg/kg body weight), respectively, with and without curcumin for 45 days. On 46th day the animals were killed by cervical dislocation. The cauda epididymis were removed and weighed, then was teased in normal saline to obtain spermatozoa., Main Outcome Measure(s): Sperm count, viability, and motility were assessed immediately. Sperm semidried smears were prepared on slides and stained by Papanicolaou stain to study sperm morphologic features., Result(s): There was a dose-dependent spermicidal effect of aflatoxin. Sperm count, viability, and motility were statistically significantly reduced. Different morphologic abnormalities were encountered. Treatment with curcumin along with aflatoxin ameliorated aflatoxin-induced sperm count, immobilization, and viability, and improved the morphologic characteristics of the sperm., Conclusion(s): Curcumin has an ameliorative effect on sperm parameters and improves morphologic features of sperm in mice.

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 toxicity on serum and blood 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. For serum parameters blood was collected in non-EDTA containing vails from heart of the dissected mice. Serum parameters are creatinine, protein, AST and ALT. The results revealed dose dependent increase in creatinine, AST and ALT and decrease in protein in serum parameters of mice. Treatment with curcumin along with aflatoxin ameliorates aflatoxin-induced changes in serum parameters.

The present investigation was an attempt to evaluate the effect of aflatoxin on biochemical and histopathological changes in the epididymis of mice and its possible amelioration on pre-treatment with vitamin E. Adult male albino mice were orally administered with 25 and 50 mg of aflatoxin/animal/day (750 and 1500 mg/kg body weight) for 45 days. Epididymis was isolated and processed for biochemical analysis. As compared with the control, absolute and relative epididymal weights were significantly reduced in aflatoxin-treated mice. Aflatoxin treatment caused significant, dose-dependent reduction in protein and sialic acid contents in caput and cauda epididymis than that of vehicle control. While activities of succinic dehydrogenase and adenosine triphosphatase were significantly reduced, acid phosphatase activity was significantly higher in caput and cauda epididymis of aflatoxin-treated mice than that of vehicle control. Pyknosis of epithelial cell nuclei, disorganization of epithelium, clumping of stereocilia and lumen devoid of sperms in caput and cauda epididymis were observed. Thus, pre-treatment with vitamin E (2 mg/0.2 mL olive oil/ animal/day) significantly ameliorated aflatoxin-induced changes, measured by biochemical and histopathological parameters.

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 is an attempt to evaluate the possible ameliorative effect of turmeric extracts/curcumin on aflatoxin induced hemolysis in vitro. Blood samples were collected from healthy adult human beings (25-30 years old) in EDTA vials and were used for preparation of RBC suspension in saline. Saline suspension of RBC was treated with aflatoxin (0.5-2.0 microg/mL) with and without turmeric extracts/curcumin (1-100 microg/mL). The results revealed that addition of aflatoxin (0.5-2.0 microg/mL) to RBC suspension caused significant dose-dependent increase in the rate of hemolysis. However, concurrent addition of aflatoxin (2.0 microg/mL) and extracts of turmeric and curcumin caused concentration-dependent retardation in aflatoxin-induced hemolysis.

Oral administration of 25 and 50 mg of aflatoxin in 0.2 mL olive oil/animal/day for 30 days caused dose-dependent and significantly higher lipid peroxidation in the kidney of aflatoxin-treated mice than in the controls. The levels of non-enzymatic antioxidant such as glutathione as well as the enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase and catalase were significantly lower in the kidney of aflatoxin-treated mice than in the controls. Black tea extract (2%) treatment significantly ameliorates aflatoxin-induced lipid peroxidation, which could be due to higher enzymatic and non-enzymatic antioxidants in the kidney of mice as compared with that given aflatoxin alone. These findings suggest that black tea extract treatment significantly ameliorates aflatoxin-induced lipid peroxidation in the kidney of mice.

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.

The kinetics of reduction of AFB(1) to AFB(2) and AFG(1) to AFG(2) by lactic acid has been investigated in dilute aqueous acidic solutions (pH 3.35-4.50) as a function of the concentrations of lactic acid, AFB(1), AFG(1) and hydrogen ion at 37 degrees C. The rate of the reaction was found to be first order with respect to the concentrations of lactic acid and aflatoxins and independent on hydrogen ion concentration. The experimental results are interpreted in terms of mechanisms involving an initial formation of transient oxonium intermediate, which tends to polarize the olefinic (C=C) carbon, which in turn causes the hydride abstraction from alpha-carbon atom of lactic acid in rate determining step. The proposed mechanisms involve an overall transfer of two protons and two electrons from lactic acid to AFB(1) and AFG(1) to give the corresponding reduced less toxic products AFB(2) and AFG(2) and the oxidised product pyruvic acid.

The potential of aflatoxin to affect testicular steroidogenesis and its amelioration by vitamin E was assessed in the present investigation. Oral administration of aflatoxin (25 and 50 microg/animal/day) for 45 days to adult mice caused, as compared with control, a dose-dependent significant rise in cholesterol content. However, the activities of 3beta- and 17beta-hydroxysteroid dehydrogenases and serum testosterone levels were significantly reduced in aflatoxin-treated mice as compared with the controls. Pretreatment with vitamin E (2 mg/animal/day, orally) significantly ameliorated aflatoxin-induced changes as compared with aflatoxin treatment alone. The present investigation clearly indicates that vitamin E ameliorates aflatoxin-induced changes in steroidogenesis.

Aim: To assess the effect of aflatoxin on biochemical changes in the testis of mice and the possibility of amelioration by vitamin E treatment., Methods: Adult male albino mice were orally administered with 25 or 50 microg of aflatoxin/animal/day (750 or 1500 microg/kg body weight) for 45 days. The testis was isolated and processed for biochemical analysis., Results: There was a significant, dose-dependent reduction in DNA, RNA, protein, sialic acid contents and the activities of succinic dehydrogenase, adenosine triphosphatase and alkaline phosphatase in the testis of aflatoxin-treated mice as compared to the vehicle control. However, the acid phosphatase activity was significantly increased in the aflatoxin-treated mice. Vitamin E (2 mg/animal/day) treatment significantly ameliorated the aflatoxin-induced changes, except the acid and alkaline phosphatase activities in the high dose group., Conclusion: Vitamin E treatment ameliorates the aflatoxin-induced changes in the testis of mice.

Aim: To evaluate the ameliorative effect of vitamin E on aflatoxin-induced lipid peroxidation in the testis., Methods: Adult male albino mice were orally administered 25 or 50 microg of aflatoxin in 0.2 mL olive oil per d for 45 d. The testis was isolated, blotted free of blood and processed for biochemical analysis., Results: There was a dose-dependent significantly higher lipid peroxidation in the testis of aflatoxin treated mice than in the controls. The levels of non-enzymatic antioxidants such as glutathione, total and reduced ascorbic acid, as well as the activities of enzymatic antioxidants, such as superoxide dismutase, glutathione peroxidase and catalase were significantly lower in the testis of aflatoxin treated mice. Vitamin E (2 mg/d per animal; orally) pretreatment significantly ameliorates the aflatoxin-induced lipid peroxidation which could be due to higher enzymatic and non-enzymatic antioxidants in the testis of mice as compared with those given aflatoxin alone., Conclusion: Vitamin E pretreatment significantly ameliorates aflatoxin-induced lipid peroxidation in the testis of mice.

We have evaluated the ameliorative role of vitamin A on aflatoxin-induced cytotoxicity in vitro. Aflatoxin (1.95 microM)-induced hemolysis was found to be significantly reduced on addition of vitamin A (125--1250 IU/ml) in incubation medium. The decrease in hemolysis was almost dose dependent. The kinetics of reduction of AFB(1) to B(2) and AFG(1) to G(2) by vitamin A has been investigated in dilute aqueous solution at 37 degrees C. The rate of the reduction was found to be first order with respect to the concentration of vitamin A and aflatoxin concentration.

Aflatoxins containing B(1), B(2), G(1) and G(2) obtained by growing Aspergillus parasiticus on SMKY liquid medium were tested for cytotoxicity (hemolysis) on RBC suspension in the presence and absence of L-ascorbic acid (AA). The results revealed that hemolysis was significantly increased on increasing the concentration of aflatoxin (0.5-3 microg ml(-1)). It was also found that pretreatment with AA (5-100 microg ml(-1)) significantly decreased aflatoxin-induced hemolysis. The solution chemistry of the interaction of aflatoxin with AA in aqueous solutions showed enhanced conversion of AFB(1) and AFG(1) to AFB(2) and AFG(2), respectively. Hemolytic, kinetic and mechanistic aspects of the interactions of aflatoxins and AA are discussed., (Copyright 1999 John Wiley & Sons, Ltd.)

Protective effect of sex steroid hormones on aflatoxin-induced cytotoxicity on RBC (hemolysis) was examined in vitro. Addition of aflatoxin (2 micrograms/ml) in RBC suspension caused significant increase in hemolysis. Concurrent addition of aflatoxin (2 micrograms/ml) and estradiolbenzoate (100-1200 pg/ml) in RBC suspension significantly retarded aflatoxin-induced hemolysis. Similarly, addition of aflatoxin (2 micrograms/ml) along with testosterone propionate (5-60 ng/ml) in RBC suspension retarded aflatoxin-induced hemolysis. Among the two synthetic hormones studied estradiolbenzoate was more potent than testosterone propionate.