Article

Thymoquinone ameliorates the immunological and histological changes induced by exposure to imidacloprid insecticide.

Zoology Department, College of Science, King Saud University, 11451 Riyadh, Saudi Arabia.
The Journal of Toxicological Sciences (Impact Factor: 1.38). 02/2012; 37(1):1-11. DOI: 10.2131/jts.37.1
Source: PubMed

ABSTRACT Previous studies have shown that thymoquinone (TQ) exerts protective effects in some models of pesticide-induced immunotoxicity. However, no data exist regarding its possible modulatory effect during imidacloprid (IC)-induced toxicity. Therefore, the aim of this study was to investigate the impact of TQ on IC-induced immunotoxicity. Sixty adult male albino rats were divided into three groups of twenty animals each. The control group was given distilled water orally, while the IC-treated group was orally administered 0.01 LD(50 )(0.21 mg/kg body weight) of IC insecticide daily for 28 days. The animals in the third group (IC/TQ group) received the same IC dose as the IC-treated group for 28 days in addition to an intraperitoneal (I.P.) injection of TQ (1 mg/kg) once every 7 days. We found that IC induced significant increases (P < 0.05) in total leukocyte counts, total immunoglobulins (Igs) (especially IgGs), the hemagglutination of antibodies, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and malondialdehyde (MDA) compared to the control group. In contrast, significant decreases (P < 0.05) in phagocytic activity, chemokine expression and chemotaxis were observed in the IC-treated group, as were severe histopathological lesions in the liver, spleen and thymus. Notably, TQ supplementation ameliorated the biochemical, histopathological, and immunological changes induced by IC by increasing phagocytic activity, chemokinesis, chemotaxis, immunoglobulin levels, and the hemagglutination of antibodies, as well as by decreasing hepatic enzymes and serum MDA levels. Taken together, our data reveal the benefits of TQ supplementation for ameliorating IC toxicity by decreasing oxidative stress and enhancing immune efficiency.

Download full-text

Full-text

Available from: Gamal Badr, Jul 06, 2015
2 Followers
 · 
329 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Human exposure to imidacloprid is likely to occur during its use as an acaricide or an ectoparasiticide. Accordingly, the developmental immunotoxic potential of imidacloprid was investigated. Oral exposure was initiated in timed pregnant female Wistar rats on gestation day 6 (GD 6) till GD 21. On GD 20, half of the gravid dams were sacrificed, and in utero fetal development was assessed. In the other half of the dams, administration was continued till weaning on postnatal day 21 (PND 21) and maternal toxicity was investigated. A subgroup of weaned pups was sacrificed to assess immunotoxicity parameters. The other half of the pups were exposed to imidacloprid till PND 42, and immunotoxicity was assessed. The findings revealed post-implantation loss in the highest dose group, indicating the risk of abortion. Soft tissue abnormalities and skeletal alterations were observed in the highest dose group. Humoral immunity was assessed by estimating hemagglutination titer and immunoglobulin production. Cell mediated immunity was assessed by Delayed Type Hypersensitivity, whereas, non-specific immunity was assessed by phagocytic index, and other phenotypic parameters. These data revealed that imidacloprid caused age-dependent adverse effects on the developing immunity which was aggravated when exposure continued throughout development, leading to a compromised immune system.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 09/2012; 51:61–70. DOI:10.1016/j.fct.2012.09.009
  • [Show abstract] [Hide abstract]
    ABSTRACT: Imidacloprid, a neonicotinoid insecticide has been in use worldwide for several years in agriculture and veterinary medicine. It is possible that residue of this compound may be recycled in the food chain and thus information regarding effects from potential exposure to it is warranted. The objective of the present study was to evaluate immunotoxic effects of imidacloprid in female BALB/c mice. Imidacloprid was administered orally daily at 10, 5, or 2.5mg/kg over 28 days. Specific parameters of humoral and cellular immune response including hemagglutinating antibody (HA) titer to sheep red blood cells (SRBC; T-dependent antigen), delayed type hypersensitivity (DTH) response to SRBC, and T-lymphocyte proliferation in response to phytohemagglutinin (PHA) were evaluated. The results showed that imidacloprid at high dose, specifically suppressed cell-mediated immune response as was evident from decreased DTH response and decreased stimulation index of T-lymphocytes to PHA. At this dose, there were also prominent histopathological alterations in spleen and liver. Histopathological analysis of footpad sections of mice revealed dose-related suppression of DTH response. Imidacloprid at low dose of 2.5mg/kg/day did not produce any significant alterations in cellular and humoral immune response and it seemed to be an appropriate dose for assessment of 'no observable adverse effects level' for immunotoxicity in BALB/c mice. The results also indicated that imidacloprid has immunosuppressive effects at doses >5mg/kg, which could potentially be attributed to direct cytotoxic effects of IMD against T cells (particularly TH cells) and that long-term exposure could be detrimental to the immune system.
    Environmental Toxicology and Pharmacology 02/2013; 35(3):408-418. DOI:10.1016/j.etap.2013.01.012
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the present study, the effects of oral administration of imidacloprid for 4 weeks on serum biochemical, oxidative stress, histopathological and ultrastructural alterations were assessed in the liver of male rats. This study also aimed to investigate whether vitamin C could protect against the imidacloprid-induced oxidative stress. Forty-eight male Sprague dawley rats were divided into four groups of 12 animals each. Group 1 served as the control, while groups 2 and 4 were administered with imidacloprid (80 mg/kg body weight) daily by oral gavage for 28 days. In addition to imidacloprid, group 4 also received vitamin C at 10 mg/kg daily by oral gavage for 28 days. Group 3 was maintained as the vitamin C control (dose as above). The serum biochemical assays revealed a significant (P < 0.05) increase in alanine transaminase and aspartate transaminase and decrease in total protein in group 2. The tissue biochemical profile revealed a significant (P < 0.05) reduction in reduced glutathione concentration in the liver of group 2 animals. Histologically, the liver showed marked dilation, congestion of central vein, portal vein and sinusoidal spaces, vacuolation/fatty change and degenerated hepatocytes. Ultra thin sections of the liver revealed swollen nuclei, varied size and shape of mitochondria, disrupted chromatin and rough endoplasmic reticulum. Co-treatment with vitamin C significantly (P < 0.05) reversed the imidacloprid-induced changes.
    03/2013; 4(1):63-7. DOI:10.4103/0976-9668.107262