Dibutyl phthalate induces oxidative stress and impairs spermatogenesis in adult rats

Aly, Hamdy A.A.; Hassan, Mostafa I.; El-Beshbishy, Hesham A.; Alahdal, Abdulrahman M.; Osman, Amira

doi:10.1177/0748233714566877

Cited by 94 publications

(67 citation statements)

References 75 publications

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“…Several animal toxicology studies report that a number of phthalates are testicular toxicants and impair spermatogenesis (Aly et al ., 2015; Uren-Webster et al ., 2010). Based on results in several animal species DEHP and DBP metabolites appear to have the capacity to disrupt normal reproduction (semen quality, etc.)…”

Section: Discussionmentioning

confidence: 99%

Phthalate exposure and semen quality in fertile US men

et al. 2015

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Several experimental and observational studies have demonstrated the antiandrogenicity of several phthalates. However, there is limited evidence of an association between phthalate exposure in adult life and semen quality. The aim of this study was to examine phthalate exposure during adulthood in relation to semen quality in fertile US men. This multi-center cross-sectional study included 420 partners of pregnant women who attended a prenatal clinic in one of five U.S. cities during 1999–2001. Nine phthalate metabolites [mono (2-ethylhexyl) phthalate (MEHP), mono (2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono (2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono (2-ethyl-5-carboxypentyl) phthalate (MECPP)], as well as mono-n-butyl phthalate (MBP) and mono-isobutyl phthalate (MiBP), mono (3 carboxypropyl) phthalate (MCPP), monobenzyl phthalate (MBzP) and monoethyl phthalate (MEP)] were measured in urine collected at the same time as the semen sample. We regressed natural log-transformed (ln) sperm concentration, ln(total sperm count), ln(total motile sperm count), percent motile sperm and percent sperm with normal morphology on each of the nine natural log-transformed metabolite concentrations and on the molar-weighted sum of DEHP metabolites in separate models. We fit unadjusted models and models that adjusted for confounders determined a priori. In unadjusted models, ln(MiBP) was significantly and positively associated with motility and ln(MBzP) significantly negatively associated with ln(total sperm count). In adjusted linear models, urinary metabolite concentrations of DEHP, DBP, DEP, and DOP were not associated with any semen parameter. We found an inverse association between ln(MBzP) concentrations and sperm motility (β = −1.47, 95% CI: −2.61, −0.33), adjusted for ln(creatinine concentration), geographic location, age, race, smoking status, stress, recent fever, time from sample collection and time to complete analysis. Several sensitivity analyses confirmed the robustness of these associations. This study and the available literature suggest that impacts of adult exposure to phthalates at environmental levels on classical sperm parameters are likely to be small.

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Section: Discussionmentioning

confidence: 99%

Phthalate exposure and semen quality in fertile US men

et al. 2015

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“…Some phthalates and phthalate metabolites have demonstrated anti‐androgenic properties in both animals and humans. Administration of the most commonly used plasticizer, dibutyl phthalate (DBP) to rats decreased serum FSH and testosterone levels, testicular weights, and sperm counts in a dose‐dependent manner (Aly et al ., ). Furthermore, these rats were found to exhibit increased oxidative stress and decreased antioxidant capacity within the testes along with associated testicular atrophy (Aly et al ., ).…”

Section: Ambient and Other Occupational Exposuresmentioning

confidence: 97%

Chronic exposures and male fertility: the impacts of environment, diet, and drug use on spermatogenesis

2016

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SUMMARYSeveral recent studies have suggested that sperm concentrations and semen quality have been decreasing over the past several decades in many areas of the world. The etiology of these decreases is currently unknown. Acute events can have significant impacts on spermatogenesis and are often readily identified during the male fertility evaluation. The majority of male factor infertility, however, is idiopathic. Chronic, low-dose exposures to chemicals and nutrients are more difficult to identify, but are extremely prevalent. These exposures have been shown to have dramatic effects on both individual and community health and interest in the cumulative and synergistic impacts of such agents on spermatogenesis has been increasing. While our understanding of these potential hazards is evolving, it is clear that they may significantly influence male reproductive potential. This review explores the literature related to effects of chronic exposures from drug use, dietary intake, and the environment on spermatogenesis in humans and animals.

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“…Another study found that oral administration of various doses of DBP to adult male albino rats was associated not only with the hormone and semen changes already mentioned but also with a dose-dependent increase in seminal oxidative stress (reduced total antioxidant capacity) in comparison with healthy controls. Exposure to the highest doses (600 µg/kg) also provoked histological alterations to the seminiferous tubules, namely absence of spermatogenic cells in some of the tubules and tubular necrosis [74]. In a later study, adult male Wistar rats exposed to different concentrations of DBP via intraperitoneal injection presented dose-dependent seminal, steroidogenic and histological alterations with a reduction in the number of conceived embryos, an increase in abortions and a reduction in litter size compared with unexposed healthy controls [75].…”

Section: Postnatal Exposure: Are There Repercussions For Adult Testicmentioning

confidence: 99%

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

Pallotti

Pelloni

Gianfrilli

et al. 2020

JCM

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Great attention has been paid in recent years to the harmful effects of various chemicals that interfere with our natural hormone balance, collectively known as endocrine-disrupting chemicals (EDCs) or endocrine disruptors. The effects on the reproductive system of bisphenol A (BPA) and phthalates have received particular attention: while they have a short half-life, they are so widespread that human exposure can be considered as continuous. Evidence is often limited to the animal model, disregarding the likelihood of human exposure to a mixture of contaminants. Data from animal models show that maternal exposure probably has harmful effects on the male fetus, with an increased risk of urogenital developmental abnormalities. After birth, exposure is associated with changes in the hypothalamic-pituitary-testicular axis, hindering the development and function of the male genital pathways through the mediation of inflammatory mechanisms and oxidative stress. The epidemiological and clinical evidence, while generally confirming the association between reproductive abnormalities and some phthalate esters and BPA, is more contradictory, with wildly different findings. The aim of this review is therefore to provide an update of the potential mechanisms of the damage caused by BPA and phthalates to reproductive function and a review of the clinical evidence currently available in the literature.

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Dibutyl phthalate induces oxidative stress and impairs spermatogenesis in adult rats

Cited by 94 publications

References 75 publications

Phthalate exposure and semen quality in fertile US men

Phthalate exposure and semen quality in fertile US men

Chronic exposures and male fertility: the impacts of environment, diet, and drug use on spermatogenesis

Mechanisms of Testicular Disruption from Exposure to Bisphenol A and Phtalates

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