Abstract Some organs in animals and human being such as ; liver , intestine and lung contain specific chemicals and active enzymes responsible for biochemical detoxification mechanisms against intoxicating agents. Glutathione is the famous chemical compound which is the substrate for glutathione peroxidase and glutathione – S – transeferase for the phase (II) of the general xenobiotic detoxificating mechanisms . This glutathione is consumed during these reactions and could be restablished by mainly sulfur containing compounds (total thiols). Aflatoxicosis is the most threating environmental condition for health community and animal wealth which is one of the highly interesting field of investigation . This submitted work has been designed in order to deduce the relationship between the level of GSH in these organs during the consecutive exposure to aflatoxicosis and the activity of these enzymes. The exposed rats day after day (for five weeks) to digestive doses of AFB1 (60μg /kg b.w.) showed that the tissue organs were increasingly enriched by accumulated lipid peroxide as a result of intoxication. This cellular peroxidation reactions ( by tissue cytochrome p450) simultaneously showed characteristic histological collaps especially in the lung tissue. The glutathione peroxidase and transeferase were concomitantly diminished by further intoxication . Conclusively; chronic intoxication by aflatoxinB1 consumed the biological reducing glutathione and total thiols as well as the acting peroxidase and transeferase.

Abstract Some organs in animals and human being such as ; liver , intestine and lung contain specific chemicals and active enzymes responsible for biochemical detoxification mechanisms against intoxicating agents. Glutathione is the famous chemical compound which is the substrate for glutathione peroxidase and glutathione – S – transeferase for the phase (II) of the general xenobiotic detoxificating mechanisms . This glutathione is consumed during these reactions and could be restablished by mainly sulfur containing compounds (total thiols). Aflatoxicosis is the most threating environmental condition for health community and animal wealth which is one of the highly interesting field of investigation . This submitted work has been designed in order to deduce the relationship between the level of GSH in these organs during the consecutive exposure to aflatoxicosis and the activity of these enzymes. The exposed rats day after day (for five weeks) to digestive doses of AFB1 (60μg /kg b.w.) showed that the tissue organs were increasingly enriched by accumulated lipid peroxide as a result of intoxication. This cellular peroxidation reactions ( by tissue cytochrome p450) simultaneously showed characteristic histological collaps especially in the lung tissue. The glutathione peroxidase and transeferase were concomitantly diminished by further intoxication . Conclusively; chronic intoxication by aflatoxinB1 consumed the biological reducing glutathione and total thiols as well as the acting peroxidase and transeferase.

Abstract Some organs in animals and human being such as ; liver , intestine and lung contain specific chemicals and active enzymes responsible for biochemical detoxification mechanisms against intoxicating agents. Glutathione is the famous chemical compound which is the substrate for glutathione peroxidase and glutathione – S – transeferase for the phase (II) of the general xenobiotic detoxificating mechanisms . This glutathione is consumed during these reactions and could be restablished by mainly sulfur containing compounds (total thiols). Aflatoxicosis is the most threating environmental condition for health community and animal wealth which is one of the highly interesting field of investigation . This submitted work has been designed in order to deduce the relationship between the level of GSH in these organs during the consecutive exposure to aflatoxicosis and the activity of these enzymes. The exposed rats day after day (for five weeks) to digestive doses of AFB1 (60μg /kg b.w.) showed that the tissue organs were increasingly enriched by accumulated lipid peroxide as a result of intoxication. This cellular peroxidation reactions ( by tissue cytochrome p450) simultaneously showed characteristic histological collaps especially in the lung tissue. The glutathione peroxidase and transeferase were concomitantly diminished by further intoxication . Conclusively; chronic intoxication by aflatoxinB1 consumed the biological reducing glutathione and total thiols as well as the acting peroxidase and transeferase.

Abstract Some organs in animals and human being such as ; liver , intestine and lung contain specific chemicals and active enzymes responsible for biochemical detoxification mechanisms against intoxicating agents. Glutathione is the famous chemical compound which is the substrate for glutathione peroxidase and glutathione – S – transeferase for the phase (II) of the general xenobiotic detoxificating mechanisms . This glutathione is consumed during these reactions and could be restablished by mainly sulfur containing compounds (total thiols). Aflatoxicosis is the most threating environmental condition for health community and animal wealth which is one of the highly interesting field of investigation . This submitted work has been designed in order to deduce the relationship between the level of GSH in these organs during the consecutive exposure to aflatoxicosis and the activity of these enzymes. The exposed rats day after day (for five weeks) to digestive doses of AFB1 (60μg /kg b.w.) showed that the tissue organs were increasingly enriched by accumulated lipid peroxide as a result of intoxication. This cellular peroxidation reactions ( by tissue cytochrome p450) simultaneously showed characteristic histological collaps especially in the lung tissue. The glutathione peroxidase and transeferase were concomitantly diminished by further intoxication . Conclusively; chronic intoxication by aflatoxinB1 consumed the biological reducing glutathione and total thiols as well as the acting peroxidase and transeferase.

Mercaptomethylpyrazolopyrimidine (2) was synthesized and reacted with ethyl chloroacetate to afford ethyl pyrazolpyrimidinylmethylmercapto acetate (3), which in turn was converted into the corresponding carbohydrazide 4. Carbohydrazide 4 reacts with a variety of reagents to give different pyrazolopyrimidines (5–12). Chloromethyl-pyrazolopyrimidine (1) reacts with chloropyridine to give compound 13, which was subjected in a series of reactions to give new compounds 14–20.