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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Joseph P, Shivanandappa T, Narasimhamurthy K, Krishnakumari M K

Toxicology Unit, Central Food Technological Research Institute, Mysore, India.

Gen Pharmacol. 1992 Nov;23(6):1159-64. doi: 10.1016/0306-3623(92)90305-4.

Technical hexachlorocyclohexane (HCH) depleted hepatic stores of vitamin A in male albino rats to cause secondary vitamin A deficiency. 2. Toxicity of HCH in rats is augmented by dietary vitamin A-deficiency as evidenced by growth retardation, organ hypertrophies and alterations in the serum and liver levels of the marker enzymes of toxicity. 3. Supplementation of dietary vitamin A to the rats either in adequate (2000 IU/kg diet) or in an excess but not hypervitaminotic level (10(5) IU/kg diet) resulted in significant protection against the toxicity of HCH. 4. The activities of the hepatic xenobiotic metabolizing enzymes were generally low (with the exception of glutathione S-transferase) in the vitamin A-deficient rats compared to those of the vitamin A supplemented diet groups. 5. The results indicated that dietary vitamin A influences the response of male albino rats to HCH toxicity possibly by modulating the activities of hepatic xenobiotic metabolizing enzymes.

工业用六氯环己烷（HCH）使雄性白化大鼠肝脏中的维生素A储备减少，导致继发性维生素A缺乏。2. 饮食中维生素A缺乏会增强HCH对大鼠的毒性，生长迟缓、器官肥大以及毒性标志物酶的血清和肝脏水平变化都证明了这一点。3. 给大鼠补充适量（2000国际单位/千克饲料）或过量但未达到维生素过多水平（10⁵国际单位/千克饲料）的饮食维生素A，可显著预防HCH的毒性。4. 与补充维生素A的饲料组相比，维生素A缺乏的大鼠肝脏中异生物质代谢酶的活性通常较低（谷胱甘肽S-转移酶除外）。5. 结果表明，饮食中的维生素A可能通过调节肝脏异生物质代谢酶的活性来影响雄性白化大鼠对HCH毒性的反应。

Joseph P, Shivanandappa T, Narasimhamurthy K, Krishnakumari M K

Toxicology Unit, Central Food Technological Research Institute, Mysore, India.

Gen Pharmacol. 1992 Nov;23(6):1159-64. doi: 10.1016/0306-3623(92)90305-4.

Technical hexachlorocyclohexane (HCH) depleted hepatic stores of vitamin A in male albino rats to cause secondary vitamin A deficiency. 2. Toxicity of HCH in rats is augmented by dietary vitamin A-deficiency as evidenced by growth retardation, organ hypertrophies and alterations in the serum and liver levels of the marker enzymes of toxicity. 3. Supplementation of dietary vitamin A to the rats either in adequate (2000 IU/kg diet) or in an excess but not hypervitaminotic level (10(5) IU/kg diet) resulted in significant protection against the toxicity of HCH. 4. The activities of the hepatic xenobiotic metabolizing enzymes were generally low (with the exception of glutathione S-transferase) in the vitamin A-deficient rats compared to those of the vitamin A supplemented diet groups. 5. The results indicated that dietary vitamin A influences the response of male albino rats to HCH toxicity possibly by modulating the activities of hepatic xenobiotic metabolizing enzymes.

工业用六氯环己烷（HCH）使雄性白化大鼠肝脏中的维生素A储备减少，导致继发性维生素A缺乏。2. 饮食中维生素A缺乏会增强HCH对大鼠的毒性，生长迟缓、器官肥大以及毒性标志物酶的血清和肝脏水平变化都证明了这一点。3. 给大鼠补充适量（2000国际单位/千克饲料）或过量但未达到维生素过多水平（10⁵国际单位/千克饲料）的饮食维生素A，可显著预防HCH的毒性。4. 与补充维生素A的饲料组相比，维生素A缺乏的大鼠肝脏中异生物质代谢酶的活性通常较低（谷胱甘肽S-转移酶除外）。5. 结果表明，饮食中的维生素A可能通过调节肝脏异生物质代谢酶的活性来影响雄性白化大鼠对HCH毒性的反应。