DNA damage in human breast milk cells and its induction by  early  and  late  milk extracts

Martin, Francis L.; Cole, Kathleen J.; Harvey, David; Weaver, Gillian; Williams, Julia; Millar, Barbara C.; Phillips, David H.; Grover, Philip L.

doi:10.1093/carcin/21.4.799

Cited by 18 publications

(10 citation statements)

References 19 publications

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“…For cell viability, the inter-individual variation was greater than the intra-individual variation. It is noteworthy that cell viabilities were high (75–100%), which is in agreement with previous literature [30]. In some participants, pre-feed cell and fat levels were higher in the control breast than in the feeding breast, demonstrating that these individuals started the sampling with a fuller feeding breast [2].…”

Section: Discussionsupporting

confidence: 91%

Breastmilk Cell and Fat Contents Respond Similarly to Removal of Breastmilk by the Infant

et al. 2013

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Large inter- and intra-individual variations exist in breastmilk composition, yet factors associated with these variations in the short-term are not well understood. In this study, the effects of breastfeeding on breastmilk cellular and biochemical content were examined. Serial breastmilk samples (∼5 mL) were collected from both breasts of breastfeeding women before and immediately after the first morning breastfeed, and then at 30-minute intervals for up to 3 hours post-feed on 2–4 mornings per participant. The infant fed from one breast only at each feed. Effects of pump versus hand expression for samples were evaluated. A consistent response pattern of breastmilk cell and fat contents to breastmilk removal was observed. Maximum fat and cell levels were obtained 30 minutes post-feed (P<0.01), with up to 8-fold increase in fat and 12-fold increase in cell content compared to the pre-feed values, and then they gradually decreased. Breastmilk cell viability and protein concentration did not change with feeding (P>0.05), although large intra-individual variability was noted for protein. Expression mode for samples did not influence breastmilk composition (P>0.05). It is concluded that breastmilk fat content, and thus breast fullness, is closely associated with breastmilk cell content. This will now form the basis for standardization of sampling protocols in lactation studies and investigation of the mechanisms of milk synthesis and cell movement into breastmilk. Moreover, these findings generate new avenues for clinical interventions exploring growth and survival benefits conferred to preterm infants by providing the highest in fat and cells milk obtained at 30 min post-expression.

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Section: Discussionsupporting

confidence: 91%

Breastmilk Cell and Fat Contents Respond Similarly to Removal of Breastmilk by the Infant

et al. 2013

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“…Association between endogenous DNA damage in lymphocytes and 17β-estradiol concentration in circulation can partially explain the inter-individual variation of the extent of endogenous DNA damage in lymphocytes from healthy donors, as reported in many studies (Buschfort et al, 1997;Martin et al, 2000;Gonzalez et al, 2002). Also, involvement of polymorphism of genes responsible for the detoxifying pathways in the induction of endogenous DNA damage should not be ignored.…”

Section: Resultsmentioning

confidence: 98%

The level of endogenous DNA damage in lymphocytes isolated from blood is associated with the fluctuation of 17beta-estradiol concentration in the follicular phase of healthy young women.

et al. 2005

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The aim of this study was to evaluate whether the differences in plasma 17beta-estradiol concentration in early and late follicular phases of the menstrual cycle can affect the level of endogenous DNA damage in lymphocytes assessed by comet assay, and whether the extent of this damage in the follicular phase is associated with the genotype of catechol-O-methyltransferase (COMT). The level of DNA damage was positively correlated with 17beta-estradiol concentration only in the late follicular phase. Subjects with the COMT L/L homozygous mutated variant revealed more DNA damage as compared to individuals with the COMT wild-type and heterozygous (H/L+HH) genotype.

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“…It has been shown that fat from about half of the women undergoing breast-reduction surgery contains a group of unidentified chemicals capable of causing DNA strand-breaks in breast epithelial cells [6]. A similar group of unidentified toxicants were reported in a similar portion of breast-milk specimens [7,8]. The mutagens in breast milk are genotoxic to epithelial cells in culture without affecting cell viability [9].…”

Section: Introductionmentioning

confidence: 91%

Genotoxicity profiles in exfoliated human mammary cells recovered from lactating mothers in Istanbul; relationship with demographic and dietary factors

Yılmaz¹,

Sandal²,

Ayvaci³

et al. 2012

Mutation Research/Genetic Toxicology and Environmental Mutagene

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DNA damage in human breast milk cells and its induction by early and late milk extracts

Cited by 18 publications

References 19 publications

Breastmilk Cell and Fat Contents Respond Similarly to Removal of Breastmilk by the Infant

Breastmilk Cell and Fat Contents Respond Similarly to Removal of Breastmilk by the Infant

The level of endogenous DNA damage in lymphocytes isolated from blood is associated with the fluctuation of 17beta-estradiol concentration in the follicular phase of healthy young women.

Genotoxicity profiles in exfoliated human mammary cells recovered from lactating mothers in Istanbul; relationship with demographic and dietary factors

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