Study of dihydroxyacetone effect on acute aluminum phosphide cardiotoxicity in albino rats.

Abstract

Aluminum phosphide (ALP) toxicity is a prevalent public health problem that induces severe damage in heart tissue. Dihydroxyacetone (DHA) is a simple saccharide naturally produced in the body and derived from plant sources, it is used as antidote against toxins caused mitochondrial death due to its ability to improves mitochondrial function and ATP depletion. The current study investigates the possible cardio protective role of DHA in ALP- intoxicated male albino rats. Rats were divided into four groups: control, DHA, ALP, and combined (ALP+DHA) groups. Arterial blood pressure (ABP), heart rate (HR), electrocardiogram (ECG) and survival time were recorded. Biochemical analysis of blood, histological study and immunohistochemistry assessment of heart tissues were done.ALP- intoxicated rats showed significant decrease in ABP, HR, survival time, catalase with ECG changes, and significant increase in serum levels of cardiac biomarkers, {troponin I and creatine kinase-MB (CK-MB)}, malondialdehyde (MDA), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) compared to control group. DHA co administration with ALP resulted in significant improvement in ABP, HR, and ECG parameters; significant decrease of cardiac biomarkers, MDA, TNF-α; and significant increase of survival time and catalase compared with the ALP- intoxicated rats. Immunohistochemistry showed upregulation of BAX, HIF-1 α and iNOS in ALP intoxicated rats. DHA coadministration with ALP group showed downregulation of BAX, HIF-1 α and iNOS.ConclusionDHA has a potential protective role against cardiac damage caused by acute ALP toxicity, therefore, its administration in cases of ALP poisoning together with other supportive therapies can improve their outcome.