Glyphosate-based herbicide causes spermatogenesis disorder and spermatozoa damage of the Chinese mitten crab (Eriocheir sinensis) by affecting testes characteristic enzymes, antioxidant capacities and inducing apoptosis
“…GSH is a crucial antioxidant in living organisms, effectively neutralizing free radicals. MDA is a metabolite of lipid peroxidation and serves as an indicator of oxidative damage in cells [45]. A dose-response relationship was observed between the concentration of butachlor and the MDA content in the gills and hepatopancreas.…”
The Chinese mitten crab (Eriocheir sinensis) is one of the most commercially important crustacean species in China. The aim of this study was to characterize the toxic effects of butachlor (an herbicide of the acetanilide class) on juvenile E. sinensis crabs. The lethal effects and the acute toxicity of butachlor on juvenile E. sinensis specimens were assessed through a semi-static in vitro experiment. We determined the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the levels of glutathione (GSH) and malondialdehyde (MDA) in the gills and the hepatopancreas of the juvenile crabs, at different time points over a 14-day short-term exposure to butachlor. Moreover, we measured the residual levels of butachlor in three different tissues (gills, hepatopancreas, and muscles) of the juvenile crabs over a longer period. Our findings revealed that butachlor is highly toxic for juvenile E. sinensis crabs. In fact, the median lethal concentration (LC50) values of butachlor at 24, 48, 72, and 96 h were found to be 4.22, 1.84, 0.34, and 0.14 mg/L, respectively, while the safe concentration was 0.014 mg/L. The antioxidant defense ability of the juvenile E. sinensis crabs against butachlor was induced after exposure to the herbicide at a concentration of 0.01 mg/L. After 14 days of exposure to butachlor at 0.04 and 0.16 mg/L, both SOD and CAT were found to be significantly inhibited (p < 0.05), the GSH levels were found to be significantly decreased (p < 0.05) and the MDA levels were identified as significantly increased (p < 0.05). Moreover, after 14 days of exposure to butachlor at 0.16 mg/L, the activities of SOD and CAT as well as the content of GSH in the hepatopancreas were found to be significantly decreased (p < 0.05). Our results revealed that a high concentration of butachlor was capable of inducing oxidative stress and damage in juvenile E. sinensis crabs. The maximal residual value of butachlor was obtained in the gills, with a content of 4.56 μg/kg. Butachlor was not detected after 24 days in the aforementioned three tissues of the juvenile crabs, thereby indicating that it was effectively metabolized.
“…GSH is a crucial antioxidant in living organisms, effectively neutralizing free radicals. MDA is a metabolite of lipid peroxidation and serves as an indicator of oxidative damage in cells [45]. A dose-response relationship was observed between the concentration of butachlor and the MDA content in the gills and hepatopancreas.…”
The Chinese mitten crab (Eriocheir sinensis) is one of the most commercially important crustacean species in China. The aim of this study was to characterize the toxic effects of butachlor (an herbicide of the acetanilide class) on juvenile E. sinensis crabs. The lethal effects and the acute toxicity of butachlor on juvenile E. sinensis specimens were assessed through a semi-static in vitro experiment. We determined the activities of superoxide dismutase (SOD) and catalase (CAT) as well as the levels of glutathione (GSH) and malondialdehyde (MDA) in the gills and the hepatopancreas of the juvenile crabs, at different time points over a 14-day short-term exposure to butachlor. Moreover, we measured the residual levels of butachlor in three different tissues (gills, hepatopancreas, and muscles) of the juvenile crabs over a longer period. Our findings revealed that butachlor is highly toxic for juvenile E. sinensis crabs. In fact, the median lethal concentration (LC50) values of butachlor at 24, 48, 72, and 96 h were found to be 4.22, 1.84, 0.34, and 0.14 mg/L, respectively, while the safe concentration was 0.014 mg/L. The antioxidant defense ability of the juvenile E. sinensis crabs against butachlor was induced after exposure to the herbicide at a concentration of 0.01 mg/L. After 14 days of exposure to butachlor at 0.04 and 0.16 mg/L, both SOD and CAT were found to be significantly inhibited (p < 0.05), the GSH levels were found to be significantly decreased (p < 0.05) and the MDA levels were identified as significantly increased (p < 0.05). Moreover, after 14 days of exposure to butachlor at 0.16 mg/L, the activities of SOD and CAT as well as the content of GSH in the hepatopancreas were found to be significantly decreased (p < 0.05). Our results revealed that a high concentration of butachlor was capable of inducing oxidative stress and damage in juvenile E. sinensis crabs. The maximal residual value of butachlor was obtained in the gills, with a content of 4.56 μg/kg. Butachlor was not detected after 24 days in the aforementioned three tissues of the juvenile crabs, thereby indicating that it was effectively metabolized.
“…Previous studies have revealed that GBH exposure triggered a dose‐dependent decrease in serum androgen levels 12,13 . Increasing evidence indicated that GBH exerted toxic effects on reproductive parameters in male crustaceans and rodents, including testicular pathological damage, decreased sperm concentration and quality, increased sperm morphological abnormalities, and progressive sperm motility disorders 12,14,15 . Moreover, these adverse effects might be mediated through mitochondrial impairment, oxidative stress, and altered functionality of characteristic testes enzymes 15,16 .…”
Section: Introductionmentioning
confidence: 99%
“…Increasing evidence indicated that GBH exerted toxic effects on reproductive parameters in male crustaceans and rodents, including testicular pathological damage, decreased sperm concentration and quality, increased sperm morphological abnormalities, and progressive sperm motility disorders 12,14,15 . Moreover, these adverse effects might be mediated through mitochondrial impairment, oxidative stress, and altered functionality of characteristic testes enzymes 15,16 . However, other studies have reported no significant changes in the reproductive system or oxidative stress parameters in rat testes after GBH exposure 17,18 .…”
Glyphosate is a widely used herbicide that has deleterious effects on animal reproduction. However, details regarding the systematic mechanisms of glyphosate‐induced reproductive toxicity are limited. This study aimed to investigate the toxic effects of glyphosate‐based herbicide (GBH) on reproduction in mice exposed to 0 (control group), 50 (low‐dose group), 250 (middle‐dose group), and 500 (high‐dose group) mg/kg/day GBH for 30 days. Toxicological parameters, metabolomics, and transcriptomics were performed to reveal GBH‐induced reproductive toxicity. Our findings demonstrated that GBH exposure damaged mitochondrial pyknosis and the nuclear membrane of spermatogonia. GBH triggered a significant increase in sperm malformations in the high‐dose group. Omics data showed that GBH impaired the Krebs cycle and respiratory chain, blocked pyruvate metabolism and glycolysis/gluconeogenesis, and influenced the pentose phosphate pathway and nucleotide synthesis and metabolism. Overall, the multi‐omics results revealed systematic and comprehensive evidence of the adverse effects of GBH exposure, providing new insights into the reproductive toxicity of organophosphorus pesticides.
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