Genotoxicity of the some selective estrogen receptor modulators: a review

Yılmaz, Serkan; Gönenç, İ̇lknur Münevver; Yılmaz, Ebru Şebnem

doi:10.1007/s10616-014-9710-7

Cited by 10 publications

(3 citation statements)

References 60 publications

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“…Al-Jassabi et al reported the motivation of oxidative DNA damage in Balb/c male mice and some other cellular sections by tamoxifen (Al-Jassabi et al 2011). In bone marrow cells, Rodrigues et al demonstrated the induction of micronuclei, and reduction of polychromatic erythrocytes formation, in female Wistar-Hannover rats (Rodrigues et al 2012;Yilmaz et al 2014). Moreover, bone marrow depression when taking tamoxifen is a well reported symptom (Sloane 2002;Gail and Wilkes 2016).…”

Section: Introductionmentioning

confidence: 99%

Potential anti-genotoxic effect of sodium butyrate to modulate induction of DNA damage by tamoxifen citrate in rat bone marrow cells

El-Shorbagy

2016

Cytotechnology

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Sodium butyrate (SB) is one of the histone deacetylase inhibitors (HDACi's) that is recently evidenced to have a prooxidant activity and an ability to reduce hydrogen peroxide-induced DNA damage. Since the majority of estrogen receptor positive breast cancer patients are treated with tamoxifen citrate (TC), which exerts well established oxidative and genotoxic effects, thus the basic objective of this study is to determine whether SB could ameliorate or curate tamoxifen citrate-induced oxidative DNA damage and genotoxic effect in vivo through up-regulation of some antioxidant enzymes. The individual and combined effects of SB and TC have been examined on rat bone marrow cells, using Micronucleus assays (MN), Comet assay, DNA fragmentation, expression of some antioxidant genes using Real time-PCR and finally, oxidative stress analysis. SB significantly increased the mitotic activity (P < 0.05), while TC induced marked micronuclei and oxidative DNA damage, in the SB post-treatment group, the combination of SB (300 mg/kg) and TC (40 mg/kg) was able to decrease the induction of MN and oxidative DNA damage through up-regulation of Cat, Sod and Gpx1 genes significantly at (P < 0.05) more efficiently than that in the SB pre-treatment one. Therefore, we postulate that SB can be used therapeutically in combination with TC treatment to modulate TC genotoxic effect by reducing its oxidative stress, and thus being an appropriate agonist agent to combine with TC than each compound alone.

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Section: Introductionmentioning

confidence: 99%

Potential anti-genotoxic effect of sodium butyrate to modulate induction of DNA damage by tamoxifen citrate in rat bone marrow cells

El-Shorbagy

2016

Cytotechnology

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“…Moreover, previous research has confirmed that long-term TAM treatment is genotoxic, and subsequent investigations have identified various genotoxic consequences of TAM in vivo. In female Wistar-Hannover rats, induction of micronuclei and reduction of polychromatic erythrocyte production was shown in bone marrow cells [48,49]. TAM-loaded PLGA was more successful in this respect; as the concentration is increased, they show reduced absorbency, especially when treated with 200 µgmL -1 .as we demonstrated how DNA was prevented from breaking down.…”

Section: Dna Damage Assaymentioning

confidence: 54%

Novel Tamoxifen Citrate-Loaded Polymeric Nanoformulations for Improving Treatment and uses in medical applications: An In Vitro and In Vivo Study

Al-jubori

Tawfeeq

Sulaiman

2022

eijs

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Tamoxifen citrate (TAM) is one of the most regularly used therapy in hormone receptor-positive breast cancer. Although it is a successful treatment, there is a problem with its bioavailability, accordingly this study was designed to improve TAM solubility and reduce its associated toxicity. TAM-Loaded poly (D, L-lactide –co- glycolide) nanostructure (TAM-loaded PLGA) has been synthesized and employed both in vitro and in vivo experiments. The blood hemolysis induced by TAM- loaded PLGA was 4.6 % at 200 µg mL-1, indicating that this nano-construct led to increased red blood cell protection. DNA molecule integrity was assessed and results indicated that DNA strands were protected from destruction at 200 µg mL-1. The antioxidant activity of TAM-loaded PLGA exceeded the pure TAM, it showed concentration-dependent scavenging action in the 100-200 µg mL-1 range, with a maximum activity of 79.2% at 200 µg mL-1. Whereas pure TAM had a decrement of 60.57%. While the activity of positive control (Vit. C) was 92.12%. Finally, the safety of TAM-loaded PLGA was examined in vivo. The functions of the heart, liver, and kidney in male mice injected with TAM-loaded PLGA were detected. A histopathological investigation was also included. TAM-loaded PLGA offered better properties as a drug delivery system, nutritional supplements, and pharmaceutical products.

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“…The extent to which underlying conditions associated with subfertility may be causal, vs effects of the drug, has also been debated ( 17 , 36 ). Arguing against this, there is compelling evidence of risks for women using clomiphene citrate including elevated incidence of endometrial and ovarian cancer at higher doses or with prolonged use ( 10 , 12 , 71-74 ).…”

Section: Discussionmentioning

confidence: 99%

Clomiphene Citrate Administered in Periconception Phase Causes Fetal Loss and Developmental Impairment in Mice

Chin,

Chan,

Kieffer

et al. 2024

Endocrinology

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Clomiphene citrate is a common treatment for ovulation induction in subfertile women, but its use is associated with elevated risk of adverse perinatal outcomes and birth defects. To investigate the biological plausibility of a causal relationship, this study investigated in mice the consequences for fetal development and pregnancy outcome of peri-conception clomiphene citrate administration at doses approximating human exposures. A dose-dependent adverse effect of clomiphene citrate given twice in the 36 h after mating was seen, with a moderate dose of 0.75 mg/kg sufficient to cause altered reproductive outcomes in three independent cohorts. Viable pregnancy was reduced by 30%, late gestation fetal weight was reduced by 16%, and ∼30% of fetuses exhibited delayed development and/or congenital abnormalities not seen in control dams, including defects of the lung, kidney, liver, eye, skin, limbs, and umbilicus. Clomiphene citrate also caused a 30 h average delay in time of birth, and elevated rate of pup death in the early postnatal phase. In surviving offspring, growth trajectory tracking and body morphometry analysis at 20 weeks of age showed post-weaning growth and development comparable to controls. A dysregulated inflammatory response in the endometrium was observed and may contribute to the underlying pathophysiological mechanism. These results demonstrate that in utero exposure to clomiphene citrate during early pregnancy can inhibit implantation and impact fetal growth and development, causing adverse perinatal outcomes. The findings raise the prospect of similar iatrogenic effects in women where clomiphene citrate may be present in the peri-conception phase unless its use is well-supervised.

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Genotoxicity of the some selective estrogen receptor modulators: a review

Cited by 10 publications

References 60 publications

Potential anti-genotoxic effect of sodium butyrate to modulate induction of DNA damage by tamoxifen citrate in rat bone marrow cells

Potential anti-genotoxic effect of sodium butyrate to modulate induction of DNA damage by tamoxifen citrate in rat bone marrow cells

Novel Tamoxifen Citrate-Loaded Polymeric Nanoformulations for Improving Treatment and uses in medical applications: An In Vitro and In Vivo Study

Clomiphene Citrate Administered in Periconception Phase Causes Fetal Loss and Developmental Impairment in Mice

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