Vitamin E-Mediated Modulation of Pulmonary Toxicity and Mineral Homeostasis in Experimental Rats Exposed to Crude Oil Vapor

This study investigated the biochemical and mineral alterations in the lungs of experimental rats exposed to varying concentrations of crude oil vapor, focusing on tissue injury markers and mineral homeostasis. The experimental design included six groups (A–F) subjected to increasing exposure levels, with Group A serving as the control. Key biochemical parameters assessed included Lactate Dehydrogenase (LDH), Gamma-Glutamyl Transferase (GGT), Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST). Additionally, serum Total Protein (TP), Calcium (Ca), and Phosphorous (P) levels were evaluated to determine systemic effects. Results revealed dose-dependent increases in all enzyme activities, indicating significant tissue damage and oxidative stress. LDH levels increased significantly at higher exposure levels, with Groups E and F showing mean values of 14.76 U/L and 15.75 U/L, respectively. GGT activity exhibited a progressive rise across all groups, with Group F reaching 9.87 U/L. ALT levels showed modest increases (1.57–2.28 U/L), suggesting partial tissue protection by vitamin E. AST levels also rose significantly, peaking at 5.71 U/L in Group F, highlighting systemic toxicity. Regression analysis identified ALT (coefficient = 3.024) and GGT (coefficient = 0.909) as the most significant predictors of AST levels (R² = 0.897), underscoring the interdependence of oxidative stress and tissue injury. Mineral analysis demonstrated progressive increases in TP (0.31–0.77 g/dL), Ca (4.21–7.53 mg/dL), and P (2.30–7.07 mg/dL), indicating disruptions in mineral homeostasis potentially linked to lung tissue damage and dysfunction. The close association between elevated calcium and phosphorus levels suggests possible soft tissue calcification at higher exposure levels. In conclusion, crude oil vapor exposure induces dose-dependent pulmonary toxicity characterized by oxidative stress, tissue injury, and mineral imbalances. Although vitamin E provided partial protection, the findings highlight the need for higher antioxidant doses or combined protective strategies to mitigate the toxicological impacts of crude oil vapor exposure.

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Journal
International Journal of Pharmaceutical and Bio-Medical Science
Published
2025-03-18
DOI
https://doi.org/10.47191/ijpbms/v5-i3-01
Primary Topic
Carcinogens and Genotoxicity Assessment
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article
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article

Vitamin E-Mediated Modulation of Pulmonary Toxicity and Mineral Homeostasis in Experimental Rats Exposed to Crude Oil Vapor

Oyeyemi Adeyemi, Offor C. E, Oluwafemi Oluwafemi
International Journal of Pharmaceutical and Bio-Medical Science
Carcinogens and Genotoxicity Assessment
article

Vitamin E-Mediated Modulation of Pulmonary Toxicity and Mineral Homeostasis in Experimental Rats Exposed to Crude Oil Vapor

Oyeyemi Adeyemi, Offor C. E, Oluwafemi Oluwafemi
article en

Abstract

This study investigated the biochemical and mineral alterations in the lungs of experimental rats exposed to varying concentrations of crude oil vapor, focusing on tissue injury markers and mineral homeostasis. The experimental design included six groups (A–F) subjected to increasing exposure levels, with Group A serving as the control. Key biochemical parameters assessed included Lactate Dehydrogenase (LDH), Gamma-Glutamyl Transferase (GGT), Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST). Additionally, serum Total Protein (TP), Calcium (Ca), and Phosphorous (P) levels were evaluated to determine systemic effects. Results revealed dose-dependent increases in all enzyme activities, indicating significant tissue damage and oxidative stress. LDH levels increased significantly at higher exposure levels, with Groups E and F showing mean values of 14.76 U/L and 15.75 U/L, respectively. GGT activity exhibited a progressive rise across all groups, with Group F reaching 9.87 U/L. ALT levels showed modest increases (1.57–2.28 U/L), suggesting partial tissue protection by vitamin E. AST levels also rose significantly, peaking at 5.71 U/L in Group F, highlighting systemic toxicity. Regression analysis identified ALT (coefficient = 3.024) and GGT (coefficient = 0.909) as the most significant predictors of AST levels (R² = 0.897), underscoring the interdependence of oxidative stress and tissue injury. Mineral analysis demonstrated progressive increases in TP (0.31–0.77 g/dL), Ca (4.21–7.53 mg/dL), and P (2.30–7.07 mg/dL), indicating disruptions in mineral homeostasis potentially linked to lung tissue damage and dysfunction. The close association between elevated calcium and phosphorus levels suggests possible soft tissue calcification at higher exposure levels. In conclusion, crude oil vapor exposure induces dose-dependent pulmonary toxicity characterized by oxidative stress, tissue injury, and mineral imbalances. Although vitamin E provided partial protection, the findings highlight the need for higher antioxidant doses or combined protective strategies to mitigate the toxicological impacts of crude oil vapor exposure.

International Journal of Pharmaceutical and Bio-Medical ScienceVol. 05(03)
Federal University of Petroleum Resource Effurun (NG)
Openalex Percentile: Top 94%
Carcinogens and Genotoxicity Assessment
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