Potentiating effect of imidacloprid on arsenic-induced testicular toxicity in Wistar rats

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.

Alteration in thiols homeostasis, protein and lipid peroxidation in renal tissue following subacute oral exposure of imidacloprid and arsenic in Wistar rats

“…Co-exposure to IMI and arsenic produced more pronounced fall in TTH level (63.8%) in renal tissue as compared to control ( Table 1 ). Similar decline in TTH level have also been reported in different visceral organs in arsenic exposed rats [ [46] , [47] , [48] ].…”

“…The reduction in activities of these antioxidant enzymes might be either due to increased concentration of free radicals or decreased concentration of reduced glutathione a substrate for different antioxidant enzymes like GPx, GST and GR. Such pronounced alterations in different antioxidant parameters in different visceral organs of animals exposed concurrently to insecticides and metals have been reported [ 41 , [46] , [47] , [48] ].…”

“…Similarly exposure of different levels of arsenic in drinking water produced significant rise in levels of MDA (74.7–212.7%) and AOPP (15.0–26.3%). The increased membrane lipid and protein peroxidation have been reported in renal [ 37 , 49 , 50 ], hepatic [ 47 ] and testicular tissue [ 48 ] of rats following exposure of arsenic. Simultaneous exposure of both the toxicants produced more pronounced increase in oxidation of membrane lipids (401.2%) and proteins (40.0%) of renal tissue compared to control as well as exposure of either toxicant ( Table 1 ).…”

Polyphenol‐rich fraction ofAlchornea cordifolialeaf ameliorates arsenite‐induced infertility in male rats

“…Protein and nonprotein thiols are critical components of the antioxidant defence systems that are actively involved in the protection of important organelles through their ability to scavenge free radicals and/or provide the substrate for the enzymatic antioxidants including the superoxide dismutase and glutathione peroxidase which were also conserved, in this study, in rats treated with AF1 following sodium arsenite exposure. Exposure to Arsenic compounds has been associated with reduced level of thiols in testicular tissue of rats with consequent aggravation of oxidative stress‐mediated injury in testicular tissues (Mahajan, Verma, Raina, & Shilpa, 2018). Exposure to sodium arsenite has been reported to cause cellular cytotoxicity and downregulation of the antioxidant defence system by inducing oxidative stress in Leydig and Sertoli cells (Yilmaz, Yildizbayrak, & Erkan, 2018).…”

Thiols: Role in Oxidative Stress-Related Disorders

“…In polycystic ovary syndrome study, it has been observed that native thiol, total thiol, disulphide levels in the ovary tissues of patients with polycystic ovary syndrome do not change compared to the control group [148]. It has been determined that arsenic and imidocarb reduce the total thiol level in the testicular tissue of rats with testicular damage [149]. In a study, it was concluded that chemotherapeutic agents cause ovarian damage in women and that the reduction of thiol level is very important in the mechanism of this damage [150].…”