The aim of the study was to investigate the therapeutic effect of aqueous extracts of some traditional medicinal plants (including Camellia sinensis leaves, Carum carvi seeds, Alpinia galangal rhizomes, Boswellia serrata resins and Cenchona officinalis bark) compared to the anticancer drug, methotrexate (MTX) against aflatoxicosis induced by aflatoxin-B1 (AFB1) in both kidneys and hearts of rats. Administration of AFB1 induces oxidative stress in kidneys of AFB1-treated rats through elevating the level of malondialdehyde (MDA) and depleting the levels of tissue antioxidants, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G-6-PDH) and vitamin C. Also the result revealed that aflatoxicosis interfere with the cellular energy supply of rat hearts through its inhibitory action on some markers of energy metabolism indicated by a decrease in glucose and glycogen contents of heart and a reduction in the activities of some glycolytic enzymes, phosphogluco-isomerase (PGI), glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and lactate dehydrogenase (LDH) compared to normal healthy animals.

Supplementation of the aqueous extracts of the different plant used, effectively ameliorated the deviation induced in both kidneys and hearts of animals in response to AFB1 administration. This effect was evident through reducing MDA level and up-regulating the inhibitory effect of AFB1 on the levels of antioxidants in kidneys as well as the energetic biomarkers in hearts. However, administration of MTX to AFB1-treated rats dramatically amplified the toxic effect of aflatoxicosis, indicated by marked increment in MDA level and decrease in the levels of antioxidants in kidneys of AFB1-MTX group in relation to AFB1 group. Also the same response was found in the bioenergetic markers of hearts. From the current investigation, it can be suggested that supplementation of the extracts of the different plants presented in this study was beneficial in modulating the alterations induced in kidney and heart under the toxic effects of AFB1.