Assessment of imidacloprid toxicity on reproductive organ system of adult male rats

Abstract

In the current study it was aimed to investigate the toxicity of low doses of imidacloprid (IMI) on the reproductive organ systems of adult male rats. The treatment groups received 0.5 (IMI-0.5), 2 (IMI-2) or 8 mg IMI/kg body weight by oral gavage (IMI-8) for three months. The deterioration in sperm motility in IMI-8 group and epidydimal sperm concentration in IMI-2 and IMI-8 groups and abnormality in sperm morphology in IMI-8 were significant. The levels of testosterone (T) and GSH decreased significantly in group IMI-8 compared to the control group. Upon treatment with IMI, apoptotic index increased significantly only in germ cells of the seminiferous tubules of IMI-8 group when compared to control. Fragmentation was striking in the seminal DNA from the IMI-8 group, but it was much less obvious in the IMI-2 one. IMI exposure resulted in elevation of all fatty acids analyzed, but the increases were significant only in stearic, oleic, linoleic and arachidonic acids. The ratios of 20:4/20:3 and 20:4/18:2 were decreased and 16:1n-9/16:0 ratio was increased. In conclusion, the present animal experiments revealed that the treatment with IMI at NOAEL dose-levels caused deterioration in sperm parameters, decreased T level, increased apoptosis of germ cells, seminal DNA fragmentation, the depletion of antioxidants and change in disturbance of fatty acid composition. All these changes indicate the suppression of testicular function.

Effects of the neonicotinoid insecticide, clothianidin, on the reproductive organ system in adult male rats

“…However, in our previous study (Bal et al, 2012a), we demonstrated that CTD exposure at the no observed adverse effect level (NOAEL) dose (32 mg/kg) daily for 90 days caused significant decreases in reproductive organ weights, sperm concentration, testicular GSH level, and significant increases in some testicular fatty acid composition, cholesterol level, apoptotic germ cells, and sperm DNA fragmentation in developing male rats. In our other study (Bal et al, 2012b), we also found that the nicotinoid, imidacloprid, when administered at NOAEL dose levels, leads to testicular dysfunction, including deteriorated sperm quality, decreased testosterone level, increased apoptotic germ cells, increased sperm DNA fragmentation, and disturbed oxidant/antioxidant balance and fatty acid composition in adult male rats. However, there is no information about the effects of CTD at or below NOAEL doses on adult mammalian reproductive functions, despite their widespread use.…”

Abnormal sperm morphology in mouse germ cells after short-term exposures to acetamiprid, propineb, and their mixture

“…It has relatively low acute and chronic toxicity in mammals and there is no evidence of carcinogenicity, neurotoxicity, mutagenicity, and/or endocrine disruption. However, studies (8,9) have reported genotoxic effects for Acm and other neonicotinoid insecticides (30)(31)(32)(33). For instance, Bal et al (34) reported that the neonicotinoid clothianidin induced impairment of the male mouse reproductive system.…”

Pesticide Exposures Induce Male-Mediated Reproductive Toxicity: A Review

“…According to Das, Shaik, and Jamil (2007), phosphorus moiety in the OPs seems to be a good substrate for nucleophilic attack leading to phosphorylation of DNA which is an example of sperm DNA damage. Apoptosis and sperm DNA fragmentation were seen in male rats given Imidacloprid orally where the overwhelming production of ROS over antioxidant is the reason for these damages (Bal et al, 2012). Methyl-Parathion, a potent alkylating agent has been recognized able to change sperm chromatin condensation that leads to DNA damage where this damage may cause risk to the offspring.…”

“…Increasing the sperm cell abnormalities specifically DNA damage were reported in several cases either human exposed to Polychlorinated biphenyls (Rignell-Hydbom et al, 2005) also in animal studies exposed to Methamidophos Methyl-Parathion (Piña-Guzmán et al, 2006), Imidacloprid (Bal et al, 2012) and Fenitrothion (Taib et al, 2014). Spermatogenesis is essential for the production of offspring whereby it is regulated by an estimation of more than 2300 genes (Tamowski et al, 2010).…”

“…The book led to the national ban on DDT and other pesticides as consequences from some huge changes regarding pesticides in the US national policy (Carson, 1962). Administration of pesticides through several routes such as oral, dermal and inhalation will affect germline cells by causing DNA double-strand breaks and later might alter the offspring (Bal et al, 2012;Piña-Guzmán et al, 2006;Rignell-Hydbom et al, 2005;Taib et al, 2014). Hence, this review will only focus on the mechanisms and the evidence of pesticides induced male-mediated reproductive toxicity.…”