Therapeutic potential of polysaccharide extracted from fenugreek seeds against thiamethoxam-induced hepatotoxicity and genotoxicity in Wistar adult rats.

This study aimed to evaluate the protective effect of a polysaccharide extracted from fenugreek seeds (Trigonella foenum-graecum) (FWEP) against insecticide-thiamethoxam (TMX)-induced hepatotoxicity. Obtained data exhibited potent antioxidant and antibacterial potentialities. On other trend, in vivo, adult female rats were divided into four groups: controls; TMX (100 mg/kg of body weight); TMX + FWEP at two graded doses, respectively (100 and 200 mg/kg of body weight) for 30 d. Up to TMX treatment, our data showed a significant increase in plasma markers of hepatotoxicity including alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and in lactate dehydrogenase (LDH) activities, which is coordinated with decline in total protein and albumin levels. Remarkably, a clear sign of genotoxicity was delivered by total disruption in hematological parameters and micronucleus (MN) test shown by severe chromatin degradation. These data were also associated with oxidative stress set up, histological and DNA injuries. However, co-administration with FWEP succeeded significantly in a dose-dependent manner in reducing and healing liver's hematological and genotoxic induced by TMX injuries.

Cardiotoxicity and myocardial infarction-associated DNA damage induced by thiamethoxam in vitro and in vivo: Protective role of Trigonella foenum-graecum seed-derived polysaccharide.

The risk of pesticides on the human health and environment has drawn increasing attention. Today, new tools are developed to reduce pesticide adverse effects. This study aimed to evaluate the toxicity induced by, thiamethoxam (TMX), and the cytoprotective effect of a novel polysaccharide, named fenugreek seed water polysaccharide (FWEP) in vitro using H9c2 cardiomyoblastes and in vivo using Wistar rat model. Animals were assigned into four groups per eight rats each: group 1 served as a control group, group 2 received TMX, group 3, and group 4 received both FWEP and TMX tested at two doses (100 and 200 mg/kg, respectively). Regarding the in vitro study, our results demonstrated that TMX induced a decrease in H9c2 cell viability up to 70% with the highest concentration. In vivo, TMX injection induced marked heart damage noted by a significant increase in plasma lactate dehydrogenase, creatine phosphokinase, troponin-T, aspartate amino transferase activities, cholesterol, and triglyceride levels. Concomitant alterations in cardiac antioxidant defense system revealed depletion in the levels of glutathione and non-protein thiol and an increase in the activity of superoxide dismutase, catalase, and glutathione peroxidase. Similarly, a significant increase in heart lipid, malondialdehyde, advanced oxidation protein product and in protein carbonyls levels was also noted. In addition, heart tissues histo-architecture displayed major presence of apoptosis and necrosis as confirmed by DNA degradation. However, supplementation with FWEP alleviated heart oxidative damage and genotoxicity. In this manner, ABTS radical-scavenging activity, linoleic acid oxidation tests and heart genomic and DNA nicking assay had proved FWEP strong antioxidant potential. In conclusion, FWEP provided significant protection against TMX-induced heart injury, and could be a useful and efficient agent against cardiotoxicity and atherosclerosis.