Phytol (PHY), a diterpenoid, is known for its various bio-pharmacological activities. However, its toxicological profile has yet to be evaluated. The aim of this study was to evaluate the cytogenotoxicological profile of PHY in Wistar albino rats. Forty-five female non-pregnant rats were treated acutely and subchronically with PHY at doses of 300 and 2000 mg/kg and 30, 60 and 90 mg/kg for 14 and 28 days. Neuropharmacological, genotoxic, and mutagenic effects were investigated. The results suggest that PHY did not cause the death of rats at a dose of 2000 mg/kg, suggesting a higher range of the LD50 of this diterpenoid. Several toxicological alterations were observed in clinical and neuropharmacological parameters depending upon the doses. No hepatic histopathological changes were observed. PHY induced genotoxicity in peripheral blood, bone marrow, liver, and kidney. PHY did not show damage repair activity in peripheral blood lymphocytes. In the bone marrow, both acute and subchronic PHY treatments increased micronucleus frequency, indicating a mutagenic effect. PHY caused neuropharmacological alterations and genetic instability, possibly through the oxidative stress induction pathway.
Oxidative stress mediated cytogenotoxicological effects of phytol in wistar albino rats
Fagoonee S.;
2023
Abstract
Phytol (PHY), a diterpenoid, is known for its various bio-pharmacological activities. However, its toxicological profile has yet to be evaluated. The aim of this study was to evaluate the cytogenotoxicological profile of PHY in Wistar albino rats. Forty-five female non-pregnant rats were treated acutely and subchronically with PHY at doses of 300 and 2000 mg/kg and 30, 60 and 90 mg/kg for 14 and 28 days. Neuropharmacological, genotoxic, and mutagenic effects were investigated. The results suggest that PHY did not cause the death of rats at a dose of 2000 mg/kg, suggesting a higher range of the LD50 of this diterpenoid. Several toxicological alterations were observed in clinical and neuropharmacological parameters depending upon the doses. No hepatic histopathological changes were observed. PHY induced genotoxicity in peripheral blood, bone marrow, liver, and kidney. PHY did not show damage repair activity in peripheral blood lymphocytes. In the bone marrow, both acute and subchronic PHY treatments increased micronucleus frequency, indicating a mutagenic effect. PHY caused neuropharmacological alterations and genetic instability, possibly through the oxidative stress induction pathway.File | Dimensione | Formato | |
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