Moringa oleifera seed oil partially abrogates 2,3-dichlorovinyl dimethyl phosphate (Dichlorvos)-induced cardiac injury in rats: evidence for the role of oxidative stress.

Abstract

Cardiovascular diseases are major causes of non-infectious diseases globally. The use of pesticides hasbeen linked with the high global burden of non-communicable diseases. Despite the indiscriminate exposure to dichlorvos (DDVP) by inhalation, no report exists on its possible cardiotoxic effect. This study investigated the cardiotoxicity of DDVP exposure by inhalation and the possible role ofMoringa oleiferaseed oil. Twenty-one male rats were randomly assigned into 3 groups. Group A (control) received only standard rat diet and water ad' libitum, group B (DDVP) was exposed to DDVP via inhalation for 15min daily in addition to rat diet and water, and group C (DDVP+M. oleifera seed oil) received treatment as group B as well as 300mg/kg of M. oleifera seed oil p.o for 28days. Significant reductions in body weight gain and cardiac weight were observed inDDVP-exposed animals (p<0.05). Similarly, 28days of exposure to DDVP led to a significant increase in lactate dehydrogenase, creatinine kinase and troponin (p<0.05). DDVP-exposed rats also showed a significant increase in malondialdehyde, and a significant decline in superoxide dismutase and glutathione peroxidase (p<0.05). However, catalase was comparable in DDVP-exposed and control rats. Histopathological observations of the cardiac tissue revealed that DDVP caused marked fat degeneration and necrosis of the myocardial layer. The changes in DDVP-exposed rats were significantly, though not completely, restored by M.oleifera seed oil administration. This study provides novel mechanistic information on the cardiotoxicity of DDVP inhalation, and the antioxidant potential of M.oleifera seed oil.