Paternal exposure to arsenic resulted in oxidative stress, autophagy, and mitochondrial impairments in the HPG axis of pubertal male offspring

Ommati, Mohammad Mehdi; Heidari, Reza; Manthari, Ram Kumar; Chiranjeevi, S. Tikka; Niu, Ruiyan; Sun, Zilong; Sabouri, Samira; Zamiri, Mohammad Javad; Zaker, Ladan; Yuan, Jianchao; Zhang, J.; Wang, J.

doi:10.1016/j.chemosphere.2019.07.056

Cited by 53 publications

(30 citation statements)

References 83 publications

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“…Sperm motility, as a potential index of fertilizing ability, can adversely be affected by environmental (94,95), industrial (96,97), and pharmaceutical agents (98). In line with previous researches (20,21,(26)(27)(28)(29)(30)(31)57), we also observed a significant decrement in sperm viability, forward motility, plasma membrane integrity (HOS test), and sperm count, as well as an increment in sperm abnormality following treatment with CNTs. Severe OS along with mitochondrial dysfunction would impair the spermatogenesis and fertility through decrements in sperm viability, count, motility, and steroidogenesis, and an increment in the percentage of abnormal sperm, as well as alterations in histomorphology of the testes or accessory sex organs (20,(26)(27)(28)30).…”

Section: Discussionsupporting

confidence: 90%

“…Mitochondrial impairment due to OS induction by CNTs in the present experiment could be an essential factor in CNTinduced reproductive toxicity. There are ample data in the literature showing that the abnormal levels of cellular glutathione (oxidized/reduced GSH) are closely interconnected with the induction of OS in reproductive organs (20,21,27,29); therefore, CNT-induced decreases in reduced GSH levels, and increases in oxidized GSH level in male gonads and gametes could trigger severe OS and complications. Spermatozoa are very sensitive to peroxidation due to the high level of polyunsaturated fatty acids (PUFAs) in the plasma membrane (26,32), adversely affecting the fertility potential (26,33,34).…”

Section: Discussionmentioning

confidence: 99%

“…It is well-known that there is a close relation between reproduction and developmental toxicity. Reprotoxicity is one of the crucial parts of chemicals risk assessments by evaluating the internal organs and endocrine system (i.e., hypothalamuspituitary-gonad-sperm axis, HPG-S) (20,21). Additionally, there is a need to clarify the reproductive and developmental health effects of CNTs (18).…”

Section: Introductionmentioning

confidence: 99%

“…Oxidative stress (OS), mitochondrial impairment, and their subsequent complications seem to play crucial roles in the xenobiotics-induced reprotoxicity and consequent infertility (20,21,(24)(25)(26)(27)(28)(29)(30). High sensitivity to OS, excessive reactive oxygen species (ROS) levels, and thiobarbituric acid reactive substances (TBARS) content could dramatically affect the functions of the reproductive organs (20,21,(26)(27)(28)(29)(30)(31)(32)(33)(34). For instance, oxidative injury and DNA damage studies indicated that high doses of MWCNT could cause DNA damage in murine sperm (35).…”

Section: Introductionmentioning

confidence: 99%

“…Cellular energy metabolism is pivotal in sperm forward motility (24,25,51), and there is ample evidence showing that xenobiotics could alter mitochondrial functionality and induce severe OS in different reproductive tissues (20,21,(27)(28)(29)(30). In this regard, Xu et al (52) reported that MWCNT caused severe damages to mitochondrial DNA in spermatocytes.…”

Section: Introductionmentioning

confidence: 99%

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Spermatotoxic Effects of Single-Walled and Multi-Walled Carbon Nanotubes on Male Mice

et al. 2020

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Carbon-based nanomaterials possess a remarkably high potential for biomedical applications due to their physical properties; however, their detrimental effects on reproduction are also concerned. Several reports indicate the toxicity of carbon nanotubes (CNT); nevertheless, their impact on intracellular organelles in the male reproductive organs has not been fully elucidated. Herein, we report on the reprotoxicity of single-walled (SWCNT) and multi-walled carbon nanotubes (MWCN) on several intracellular events and histological criteria in pubertal male BALB/c mice orally treated with 0, 10, and 50 mg/kg/day doses for 5 weeks. Biomarkers of oxidative stress and mitochondrial functionality, histopathological alterations, and epididymal sperm characteristics were determined. Oral administration of CNTs at 10 and 50 mg/kg evoked a significant decrement in weight coefficient, sperm viability and motility, hypo-osmotic swelling (HOS) test, sperm count, mitochondrial dehydrogenase activity, ATP content, total antioxidant capacity, and GSH/GSSH ratio in the testis and epididymal spermatozoa. On the other hand, percent abnormal sperm, testicular and sperm TBARS contents, protein carbonylation, ROS formation, oxidized glutathione level, and sperm mitochondrial depolarization were considerably increased. Significant histopathological and stereological alterations in the testis occurred in the groups challenged with CNTs. The current findings indicated that oxidative stress and mitochondrial impairment might substantially impact CNTs-induced reproductive system injury and sperm toxicity. The results can also be used to establish environmental standards for CNT consumption by mammals, produce new chemicals for controlling the rodent populations, and develop therapeutic approaches against CNTs-associated reproductive anomalies in the males exposed daily to these nanoparticles.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Spermatotoxic Effects of Single-Walled and Multi-Walled Carbon Nanotubes on Male Mice

et al. 2020

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Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Gong

Xue

et al. 2021

Advanced Science

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The rise of metabolic disorders in modern times is mainly attributed to the environment. However, heritable effects of environmental chemicals on mammalian offsprings' metabolic health are unclear. Inorganic arsenic (iAs) is the top chemical on the Agency for Toxic Substances and Disease Registry priority list of hazardous substances. Here, we assess cross‐generational effects of iAs in an exclusive male‐lineage transmission paradigm. The exposure of male mice to 250 ppb iAs causes glucose intolerance and hepatic insulin resistance in F1 females, but not males, without affecting body weight. Hepatic expression of glucose metabolic genes, glucose output, and insulin signaling are disrupted in F1 females. Inhibition of the glucose 6‐phosphatase complex masks the intergenerational effect of iAs, demonstrating a causative role of hepatic glucose production. F2 offspring from grandpaternal iAs exposure show temporary growth retardation at an early age, which diminishes in adults. However, reduced adiposity persists into middle age and is associated with altered gut microbiome and increased brown adipose thermogenesis. In contrast, F3 offspring of the male‐lineage iAs exposure show increased adiposity, especially on a high‐calorie diet. These findings have unveiled sex‐ and generation‐specific heritable effects of iAs on metabolic physiology, which has broad implications in understanding gene‐environment interactions.

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Drug‐induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies

Ommati

Mobasheri

Heidari

2021

J Biochem & Molecular Tox

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The world is currently facing an unprecedented pandemic caused by a newly recognized and highly pathogenic coronavirus disease 2019 (COVID‐19; induced by SARS‐CoV‐2 virus), which is a severe and ongoing threat to global public health. Since COVID‐19 was officially declared a pandemic by the World Health Organization in March 2020, several drug regimens have rapidly undergone clinical trials for the management of COVID‐19. However, one of the major issues is drug‐induced organ injury, which is a prominent clinical challenge. Unfortunately, most drugs used against COVID‐19 are associated with adverse effects in different organs, such as the kidney, heart, and liver. These side effects are dangerous and, in some cases, they can be lethal. More importantly, organ injury is also a clinical manifestation of COVID‐19 infection. These adverse reactions are increasingly recognized as outcomes of COVID‐19 infection. Therefore, the differential diagnosis of drug‐induced adverse effects from COVID‐19‐induced organ injury is a clinical complication. This review highlights the importance of drug‐induced organ injury, its known mechanisms, and the potential therapeutic strategies in COVID‐19 pharmacotherapy. We review the potential strategies for the differential diagnosis of drug‐induced organ injury. This information can facilitate the development of therapeutic strategies, not only against COVID‐19 but also for future outbreaks of other emerging infectious diseases.

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Paternal exposure to arsenic resulted in oxidative stress, autophagy, and mitochondrial impairments in the HPG axis of pubertal male offspring

Cited by 53 publications

References 83 publications

Spermatotoxic Effects of Single-Walled and Multi-Walled Carbon Nanotubes on Male Mice

Spermatotoxic Effects of Single-Walled and Multi-Walled Carbon Nanotubes on Male Mice

Inter‐ and Transgenerational Effects of Paternal Exposure to Inorganic Arsenic

Drug‐induced organ injury in coronavirus disease 2019 pharmacotherapy: Mechanisms and challenges in differential diagnosis and potential protective strategies

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