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<p>The classic antipsychotic drug haloperidol is known to possess neurotoxic effects in experimental animals. The aim is to investigate neuronal injury, liver damage, and genotoxicity effects of haloperidol and their possible modulation by treatment with α-lactalbumin (Lacprodan® α-10) in the rat. Lacprodan® α-10 (100 or 200&#xa0;mg/kg) was concurrently given with haloperidol (1.5&#xa0;mg/kg) for 2&#xa0;weeks. Compared with the saline control group, rats treated with only haloperidol exhibited significantly decreased reduced glutathione concentration and superoxide dismutase activity along with raised malondialdehyde levels in both brain and liver tissue. Additionally, haloperidol caused significant structural and numerical chromosomal aberrations, increased hepatic DNA fragmentation and DNA damage of peripheral blood lymphocytes. Oral administration of Lacprodan® α-10 in a dose of 200&#xa0;mg/kg resulted in a significant increase in reduced glutathione concentration and decreased lipid peroxidation (malondialdehyde) in brain and liver tissue. Moreover, Lacprodan® α-10 (100–200&#xa0;mg/kg) resulted in a significant increase in superoxide dismutase activity compared to the haloperidol control group. Lacprodan® α-10 ameliorated the gentotoxcity and DNA damage caused by haloperidol. The histological assessment showed that haloperidol caused degenerated neurocytes, and pericellular vacuolation. The liver exhibited significant damage with necrosis of hepatocytes, focal area of lymphocyte infiltration and hemorrhage in between hepatocytes. These changes were markedly ameliorated by treatment with Lacprodan® α-10 (200&#xa0;mg/kg). Lacprodan® α-10 can prevent the neurotoxic and genotoxic/DNA damage caused by the haloperidol. Therefore, Lacprodan® α-10 is likely to prove of value in reducing these adverse effects in patients treated with haloperidol.</p>

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The protective effect of Lacprodan®alpha-10 against acute neurotoxic, hepatotoxic, and genotoxic effects induced by haloperidol

  • 期刊论文

  • 发表日期：

    2025年1月24日

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  • Mahrousa M. Hassanane Kandil,
  • Enayat A. Omara,
  • Somaia A. Nada,
  • Mayada A. El-Hiny,
  • Omar M. E. Abdel-Salam

摘要

The classic antipsychotic drug haloperidol is known to possess neurotoxic effects in experimental animals. The aim is to investigate neuronal injury, liver damage, and genotoxicity effects of haloperidol and their possible modulation by treatment with α-lactalbumin (Lacprodan® α-10) in the rat. Lacprodan® α-10 (100 or 200 mg/kg) was concurrently given with haloperidol (1.5 mg/kg) for 2 weeks. Compared with the saline control group, rats treated with only haloperidol exhibited significantly decreased reduced glutathione concentration and superoxide dismutase activity along with raised malondialdehyde levels in both brain and liver tissue. Additionally, haloperidol caused significant structural and numerical chromosomal aberrations, increased hepatic DNA fragmentation and DNA damage of peripheral blood lymphocytes. Oral administration of Lacprodan® α-10 in a dose of 200 mg/kg resulted in a significant increase in reduced glutathione concentration and decreased lipid peroxidation (malondialdehyde) in brain and liver tissue. Moreover, Lacprodan® α-10 (100–200 mg/kg) resulted in a significant increase in superoxide dismutase activity compared to the haloperidol control group. Lacprodan® α-10 ameliorated the gentotoxcity and DNA damage caused by haloperidol. The histological assessment showed that haloperidol caused degenerated neurocytes, and pericellular vacuolation. The liver exhibited significant damage with necrosis of hepatocytes, focal area of lymphocyte infiltration and hemorrhage in between hepatocytes. These changes were markedly ameliorated by treatment with Lacprodan® α-10 (200 mg/kg). Lacprodan® α-10 can prevent the neurotoxic and genotoxic/DNA damage caused by the haloperidol. Therefore, Lacprodan® α-10 is likely to prove of value in reducing these adverse effects in patients treated with haloperidol.