The effects analysis of two neonicotinoid insecticides on &lt;i&gt;in vitro&lt;/i&gt; maturation of porcine oocytes using hanging drop monoculture method

Ishikawa, Sadamasa; Hiraga, Kou; Hiradate, Yuuki; Tanemura, Kentaro

doi:10.1292/jvms.15-0008

Cited by 7 publications

(5 citation statements)

References 19 publications

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“…Importantly, significant alternations of genes associated with oocyte meiosis ( ccnb1 and cdc20 ) were observed in F1 in this research. Published studies report that IMI is detrimental to sperm function or oocyte maturation, fertilization, and subsequent development in bees, mice, and porcine. − In addition, steroid biosynthesis was significantly enriched in the THM groups in F1 generation, which were consistent with the data from the gonads in F0 generations. Interestingly, paternal/maternal exposure to IMI and THM all decreased the levels of T and E2 in F1 generations.…”

Section: Discussionmentioning

confidence: 80%

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Zhang,

Shi,

et al. 2023

Environ. Sci. Technol.

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Imidacloprid (IMI) and thiamethoxam (THM) are ubiquitous in aquatic ecosystems. Their negative effects on parental fish are investigated while intergenerational effects at environmentally relevant concentrations remain unclear. In this study, F0 zebrafish exposed to IMI and THM (0, 50, and 500 ng L −1 ) for 144 days post-fertilization (dpf) was allowed to spawn with two modes (internal mating and cross-mating), resulting in four types of F1 generations to investigate the intergenerational effects. IMI and THM affected F0 zebrafish fecundity, gonadal development, sex hormone and VTG levels, with accumulations found in F0 muscles and ovaries. In F1 generation, paternal or maternal exposure to IMI and THM also influenced sex hormones levels and elevated the heart rate and spontaneous movement rate. LncRNA−mRNA network analysis revealed that cell cycle and oocyte meiosis-related pathways in IMI groups and steroid biosynthesis related pathways in THM groups were significantly enriched in F1 offspring. Similar transcriptional alterations of dmrt1, insl3, cdc20, ccnb1, dnd1, ddx4, cox4i1l, and cox5b2 were observed in gonads of F0 and F1 generations. The findings indicated that prolonged paternal or maternal exposure to IMI and THM could severely cause intergenerational toxicity, resulting in developmental toxicity and endocrine-disrupting effects in zebrafish offspring.

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Section: Discussionmentioning

confidence: 80%

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Zhang,

Shi,

et al. 2023

Environ. Sci. Technol.

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“…However, concentrations of 30 ppm and 100 ppm significantly reduced oocyte maturation. Although the exact mode of action of ACP on oocyte maturation is unknown, occurrence of increased lipid peroxidation and decreased antioxidant factors including glutathione and super oxidase, catalase, glutathione peroxidase has been described ( Ishikawa et al ., 2015 ).…”

Section: Discussionmentioning

confidence: 99%

“…Studies have suggested that the main mechanisms for ACP-induced toxicity include increased oxidative stress, decreased activity of antioxidant systems that play a protective role in the body (ROS), and increased lipid peroxidation of membranes. Ishikawa et al (2015) evaluated the effect of ACP on the maturation of porcine oocytes in a laboratory. The results showed that oocyte nucleus maturation in the group given ACP at a concentration of 10 ppm was not significantly different from controls.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of the protective effect of melatonin on oocyte, embryo and ovarian tissue parameters in female mice exposed to acetamiprid

Hassanzadeh,

Joursaraei,

Hejazian

et al. 2023

JBRA

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Objective Acetamiprid (ACP) causes infertility and its effect appears to occur via oxidative stress. Melatonin has antioxidative properties. Thus, in this experimental study, we examined the protective effect of melatonin against toxic pathologic changes from ACP on reproductive system parameters of female mice. Methods The study included 30 female mice divided into 5 groups (6 mice in each group), as follows: Saline (control group); ACP (10, 20 mg/kg); ACP (10mg/kg) + melatonin (10mg/kg); and ACP (20mg/kg) + melatonin (10mg/kg). All mice were given intraperitoneal injections daily for one month. The groups were evaluated for ovarian histopathological changes and oocyte quality based on in vitro fertilization (IVF) parameters. Results ACP induced histological damages in the ovaries of mice and caused increases in the number of atretic follicles and decreases in the quality of oocytes based on IVF parameters. These alterations were significantly reduced by melatonin. Conclusions Melatonin can decrease the toxic effects of ACP in the female reproductive system of mice. Further studies are needed.

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“…The effects of ACE and imidacloprid on porcine oocyte maturation in vitro have been reported previously. Irregular chromosomes were observed in the ACE-or imidacloprid-exposed groups and nuclear maturation rates were significantly reduced (Ishikawa et al, 2015). Formate insecticides are commonly used.…”

Section: Pesticidesmentioning

confidence: 99%

Fertility loss: negative effects of environmental toxicants on oogenesis

et al. 2023

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There has been a global decline in fertility rates, with ovulatory disorders emerging as the leading cause, contributing to a global lifetime infertility prevalence of 17.5%. Formation of the primordial follicle pool during early and further development of oocytes after puberty is crucial in determining female fertility and reproductive quality. However, the increasing exposure to environmental toxins (through occupational exposure and ubiquitous chemicals) in daily life is a growing concern; these toxins have been identified as significant risk factors for oogenesis in women. In light of this concern, this review aims to enhance our understanding of female reproductive system diseases and their implications. Specifically, we summarized and categorized the environmental toxins that can affect oogenesis. Here, we provide an overview of oogenesis, highlighting specific stages that may be susceptible to the influence of environmental toxins. Furthermore, we discuss the genetic and molecular mechanisms by which various environmental toxins, including metals, cigarette smoke, and agricultural and industrial toxins, affect female oogenesis. Raising awareness about the potential risks associated with toxin exposure is crucial. However, further research is needed to fully comprehend the mechanisms underlying these effects, including the identification of biomarkers to assess exposure levels and predict reproductive outcomes. By providing a comprehensive overview, this review aims to contribute to a better understanding of the impact of environmental toxins on female oogenesis and guide future research in this field.

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The effects analysis of two neonicotinoid insecticides on <i>in vitro</i> maturation of porcine oocytes using hanging drop monoculture method

Cited by 7 publications

References 19 publications

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Chronic Paternal/Maternal Exposure to Environmental Concentrations of Imidacloprid and Thiamethoxam Causes Intergenerational Toxicity in Zebrafish Offspring

Evaluation of the protective effect of melatonin on oocyte, embryo and ovarian tissue parameters in female mice exposed to acetamiprid

Fertility loss: negative effects of environmental toxicants on oogenesis

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