Graphical abstract

BackgroundIt is an established fact that humans and animals are exposed to more than one chemical concurrently from various sources such as food, air and water. In the past, much emphasis was laid on evaluating the toxic effects of a single chemical. Nowadays an increased attention is being paid to the interaction of xenobiotics with one another. Therefore, a study was aimed to evaluate the potentiating effect of imidacloprid (IMI) on arsenic-induced testicular toxicity in rats.MethodsAdult male Wistar rats randomly divided into eight groups with six in each were subjected to daily oral administrations for 28 days. Group I served as control, group II received IMI at the dose rate of 16.9 mg/kg body weight, group III, IV and V received arsenic at the dose rate of 50, 100 and 150 ppb in drinking water whereas group VI, VII and VIII received both arsenic and IMI.ResultsRepeated oral administrations of IMI or arsenic (150 ppb) alone resulted in a significant (P < 0.05) elevation in the levels of malondialdehyde (MDA) and advanced oxidation protein product (AOPP) along with significant (P < 0.05) decline in total thiols and antioxidant enzymatic activities indicating reduced antioxidant defense in testicular tissue of exposed rats. These findings were further corroborated with histological alterations in testes like fluid accumulation in interstitial spaces in IMI administered rats. Similarly, rats provided access exclusively to arsenic-containing drinking water induced degenerative changes in seminiferous tubules in a concentration-dependent manner. Concurrent administration of IMI and arsenic produced more severe antioxidant and histopathological alterations of testes as compared to exposure to either toxicant.ConclusionsReduced antioxidant activities, increased MDA and AOPP levels with severe histopathological alterations in testes of rats on concurrent exposure indicated that IMI potentiated the arsenic-induced testicular toxicity in Wistar rats.

Imidacloprid (IMI), a newer neonicotinoid insecticide, induces oxidative insult to hepatocytes due to the formation of reactive metabolites during hepatic metabolism. The present study aimed to determine the potentiating effect of arsenic (As) on IMI-induced hepatic damage in Wistar rats. Rats, randomly divided into eight groups with six in each, were subjected to daily oral administration for 28 days. Group I served as control; group II received IMI at the dose rate of 16.9 mg/kg body weight; groups III, IV, and V received As at the dose rate of 50, 100, and 150 ppb, respectively, in drinking water; groups VI, VII, and VIII received both IMI (16.9 mg/kg) and As in drinking water at the rate of 50, 100, and 150 ppb, respectively. Repeated oral administration of IMI or As resulted in significant ( p < 0.05) elevation of plasma phosphatases, transferases, hepatic malondialdehyde, and advanced oxidation protein product levels, but significantly ( p < 0.05) decreased levels of total proteins, thiols, and activities of antioxidant enzymes that indicate oxidation-induced hepatotoxicity. These findings were further corroborated by histological alterations in hepatic tissue of IMI or As-administered rats. The coadministration of both IMI and As in rats produced more severe alterations in these parameters in hepatic tissue. Reduced antioxidant indices and increased hepatic damage biomarkers with pronounced histopathological alterations in hepatic tissue after combined exposure to toxicants indicate potentiating toxic effect of As on IMI-induced hepatotoxicity.