Paternal Exposure to Methylphenidate Induces Poor‐Quality Blastocyst and Epigenetic Changes

ABSTRACT Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) w...

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Published inMolecular reproduction and development Vol. 92; no. 5; pp. e70026 - n/a
Main Authors Gomes, Ana Clara da Costa Nunes, Pagliari, Laura Eduarda S. C., Stumpp, Taiza, Vendramini, Vanessa
Format Journal Article
LanguageEnglish
Published United States Wiley Subscription Services, Inc 01.05.2025
John Wiley and Sons Inc
Subjects
Animals
Blastocyst - cytology
Blastocyst - drug effects
Blastocyst - metabolism
Blastocyst - pathology
Blastocysts
DNA fragmentation
embryo
Epigenesis, Genetic - drug effects
Epigenetics
Female
histone methylation
Histones
Histones - metabolism
Immunocytochemistry
Male
Methylphenidate
Methylphenidate - adverse effects
Methylphenidate - pharmacology
Methylphenidate - toxicity
Paternal Exposure - adverse effects
psychostimulant
Rats
Rats, Wistar
spermatozoa
Spermatozoa - drug effects
toxicology
toxicology
histone methylation
embryo
spermatozoa
psychostimulant
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Abstract ABSTRACT Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% (p = 0.02), as well as increased those classified as “poor” by more than 150% (p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 (p = 0.01), a reduction of H4K20me3 (p = 0.05) and a nonsignificant increase of H3K4me3 (p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.
AbstractList Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats ( n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% ( p = 0.02), as well as increased those classified as “poor” by more than 150% ( p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 ( p = 0.01), a reduction of H4K20me3 ( p = 0.05) and a nonsignificant increase of H3K4me3 ( p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.
Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats ( n  = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% ( p  = 0.02), as well as increased those classified as “poor” by more than 150% ( p  < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 ( p  = 0.01), a reduction of H4K20me3 ( p  = 0.05) and a nonsignificant increase of H3K4me3 ( p  = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.
ABSTRACT Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% (p = 0.02), as well as increased those classified as “poor” by more than 150% (p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 (p = 0.01), a reduction of H4K20me3 (p = 0.05) and a nonsignificant increase of H3K4me3 (p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.
Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% (p = 0.02), as well as increased those classified as "poor" by more than 150% (p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 (p = 0.01), a reduction of H4K20me3 (p = 0.05) and a nonsignificant increase of H3K4me3 (p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In rats, we showed increased sperm DNA fragmentation and reduced embryonic viability. In the present report, male Wistar rats (n = 21) were divided into two groups: control and methylphenidate. The control group received 1 mL/kg of distilled water, while the methylphenidate group received 5 mg/kg by gavage from 38 to 68 days of age on a single daily dose. After this period, there was an interval before exposed rats started a mating schedule with untreated/normally cycling females. Morphological quality and key epigenetic marks in the blastocysts were assessed. Immunocytochemistry was performed in fresh blastocysts to quantify the trimethylated histones H3K4, H3K9, and H4K20. Treatment with methylphenidate reduced the mean quality of blastocysts by 43.57% (p = 0.02), as well as increased those classified as "poor" by more than 150% (p < 0.001). Epigenetic marks were also altered, with an increase in the intensity of H3K9me3 (p = 0.01), a reduction of H4K20me3 (p = 0.05) and a nonsignificant increase of H3K4me3 (p = 0.34). The results suggest that the decline in blastocyst quality is highly associated with subchronic use of this psychostimulant by adolescent males. This is the first report showing the risks posed by methylphenidate to the epigenetic signature of a mammalian blastocyst following paternal exposure.
Author Vendramini, Vanessa
Gomes, Ana Clara da Costa Nunes
Pagliari, Laura Eduarda S. C.
Stumpp, Taiza
AuthorAffiliation 1 Department of Morphology and Genetics, Laboratory of Reproductive and Developmental Biology (LaBReD) Paulista School of Medicine Federal University of Sao Paulo ‐ EPM/UNIFESP São Paulo Brazil
AuthorAffiliation_xml – name: 1 Department of Morphology and Genetics, Laboratory of Reproductive and Developmental Biology (LaBReD) Paulista School of Medicine Federal University of Sao Paulo ‐ EPM/UNIFESP São Paulo Brazil
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  givenname: Ana Clara da Costa Nunes
  orcidid: 0000-0001-7009-1807
  surname: Gomes
  fullname: Gomes, Ana Clara da Costa Nunes
  organization: Federal University of Sao Paulo ‐ EPM/UNIFESP
– sequence: 2
  givenname: Laura Eduarda S. C.
  surname: Pagliari
  fullname: Pagliari, Laura Eduarda S. C.
  organization: Federal University of Sao Paulo ‐ EPM/UNIFESP
– sequence: 3
  givenname: Taiza
  surname: Stumpp
  fullname: Stumpp, Taiza
  organization: Federal University of Sao Paulo ‐ EPM/UNIFESP
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  surname: Vendramini
  fullname: Vendramini, Vanessa
  email: vanessa.vendramini@unifesp.br
  organization: Federal University of Sao Paulo ‐ EPM/UNIFESP
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Issue 5
Keywords toxicology
histone methylation
embryo
spermatozoa
psychostimulant
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Snippet ABSTRACT Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in...
Epigenetic changes caused by methylphenidate hydrochloride on paternal inheritance have been suggested in fish, yet a subject to be determined in mammals. In...
SourceID pubmedcentral
proquest
pubmed
crossref
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Publisher
StartPage e70026
SubjectTerms Animals
Blastocyst - cytology
Blastocyst - drug effects
Blastocyst - metabolism
Blastocyst - pathology
Blastocysts
DNA fragmentation
embryo
Epigenesis, Genetic - drug effects
Epigenetics
Female
histone methylation
Histones
Histones - metabolism
Immunocytochemistry
Male
Methylphenidate
Methylphenidate - adverse effects
Methylphenidate - pharmacology
Methylphenidate - toxicity
Paternal Exposure - adverse effects
psychostimulant
Rats
Rats, Wistar
spermatozoa
Spermatozoa - drug effects
toxicology
Title Paternal Exposure to Methylphenidate Induces Poor‐Quality Blastocyst and Epigenetic Changes
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fmrd.70026
https://www.ncbi.nlm.nih.gov/pubmed/40406889
https://www.proquest.com/docview/3228948878
https://www.proquest.com/docview/3206987576
https://pubmed.ncbi.nlm.nih.gov/PMC12100459
Volume 92
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