Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring

Church, Michael W.; Jen, K.‐L. Catherine; Anumba, J.I.; Jackson, D.A.; Adams, Brittany R.; Hotra, John W.

doi:10.1016/j.ntt.2009.09.006

Cited by 46 publications

(68 citation statements)

References 83 publications

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“…We have previously found that under some conditions that high levels of DHA could be toxic (Church et al ., 2010). In order to assure that this was not the case under the conditions employed in these experiments, in figure 1 Jurkat T cells were exposed to 5 μM Hg 2+ or vehicle control .…”

Section: Resultsmentioning

confidence: 99%

Docosahexaenoic acid counteracts attenuation of CD95-induced cell death by inorganic mercury

Gill

Lanni

Jen

et al. 2015

Toxicology and Applied Pharmacology

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In the United States the principal environmental exposure to mercury is through dietary consumption of sea food. Although the mechanism by which low levels of mercury affect the nervous system is not well established, epidemiological studies suggest that low level exposure of pregnant women to dietary mercury can adversely impact cognitive development in their children, but that Docosahexaenoic acid (DHA), the most prominent n-polyunsaturated fatty acid (n-PUFA) present in fish may counteract negative effects of mercury on the nervous system. Aside from effects on the nervous system, epidemiological and animal studies have also suggested that low level mercury exposure may be a risk factor for autoimmune disease. However unlike the nervous system where a mechanism linking mercury to impaired cognitive development remains elusive, we have previously suggested a potential mechanism linking low level mercury exposures to immune system dysfunction and autoimmunity. In the immune system it is well established that disruption of CD95 mediated apoptosis leads to autoimmune disease. We have previously shown in vitro as well as in vivo that in lymphocytes burdened with low levels of mercury, CD95 mediated cell death is impaired. In this report we now show that DHA counteracts the negative effect of mercury on CD95 signaling in T lymphocytes. T cells which have been pre-exposed to DHA are able to cleave pro-caspase 3 and efficiently signal programmed cell death through the CD95 signaling pathway, whether or not they are burdened with low levels of mercury. Thus DHA may lower the risk of autoimmune disease after low level mercury exposures.

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Section: Resultsmentioning

confidence: 99%

Docosahexaenoic acid counteracts attenuation of CD95-induced cell death by inorganic mercury

Gill

Lanni

Jen

et al. 2015

Toxicology and Applied Pharmacology

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“…(3–6) On the other hand, the adverse effects of fish oil, including those reported in this study, have also been reported. (17,52–54) Accordingly, it will be necessary to further examine the ingestion level and the duration of fish oil, and to establish methods to effectively use fish oil in the future.…”

Section: Discussionmentioning

confidence: 99%

Fish oil changes the lifespan of Caenorhabditis elegans via lipid peroxidation

Sugawara¹,

Honma²,

Ito³

et al. 2013

J. Clin. Biochem. Nutr.

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Recently, we administered fish oil containing eicosapentaenoic acid and docosahexaenoic acid (DHA) to senescence-accelerated mice P8 (SAMP8), in order to investigate the effects on lifespan. Surprisingly, the lifespan of SAMP8 that were fed fish oil was shortened significantly, through a mechanism that likely involved lipid peroxidation. In this study, we investigated this phenomenon in further detail. To examine whether this phenomenon occurs only in SAMP8, we investigated the effect of fish oil on the lifespan of another organism species, Caenorhabditis elegans (C. elegans). C. elegans fed fish oil were cultured and the lifespan monitored. As a consequence of the provision of large amounts of fish oil the lifespan of C. elegans was shortened significantly, whereas an appropriate amount of fish oil extended their lifespan significantly. Lipid peroxide levels in C. elegans that were fed fish oil increased significantly in a dose-dependent manner. However, lipid peroxide levels in C. elegans were inhibited by the addition of fish oil and an antioxidant, α-tocopherol, and completely abrogated the changes in the lifespan. To further confirm whether the oxidation of n-3 polyunsaturated fatty acid in fish oil would change the lifespan of C. elegans, the effect of oxidized DHA was examined. Large amounts of oxidized DHA were found to shorten their lifespan significantly. Thus, fish oil changes the lifespan of C. elegans through lipid peroxidation.

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“…This was done at each stimulus intensity level in order to derive amplitude-intensity (A-I) profiles. Whereas the ABR amplitude is a function of neural synchrony and the number of neural units firing, the ABR amplitude can provide diagnostic information on these neural functions [26,71,89] and the presence of hyperacusis [15]. …”

Section: Methodsmentioning

confidence: 99%

Repeated antenatal corticosteroid treatments adversely affect neural transmission time and auditory thresholds in laboratory rats

Church

Adams

Anumba

et al. 2012

Neurotoxicology and Teratology

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Antenatal corticosteroid (AC) treatment is given to pregnant women at risk for preterm birth to reduce infant morbidity and mortality by enhancing lung and brain maturation. However, there is no accepted regimen on how frequently AC treatments should be given and some studies found that repeated AC treatments can cause growth retardation and brain damage. Our goal was to assess the dose-dependent effects of repeated AC treatment and estimate the critical number of AC courses to cause harmful effects on the auditory brainstem response (ABR), a sensitive measure of brain development, neural transmission and hearing loss. We hypothesized that repeated AC treatment would have harmful effects on the offspring’s ABRs and growth only if more than 3 AC treatment courses were given. To test this hypothesis, pregnant Wistar rats were given either a high regimen of AC (HAC), a moderate regimen (MAC), a low regimen (LAC), or saline (SAL). An untreated control (CON) group was also used. Simulating the clinical condition, the HAC dams received 0.2 mg/kg Betamethasone (IM) twice daily for 6 days during gestation days (GD) 17-22. The MAC dams received 3 days of AC treatment followed by 3 days of saline treatment on GD 17-19 and GD 20-22, respectively. The LAC dams received 1 day of AC treatment followed by 5 days of saline treatment on GD 17 and GD 18-22, respectively. The SAL dams received 6 days of saline treatment from GD 17-22 (twice daily, isovolumetric to the HAC injections, IM). The offspring were ABR-tested on postnatal day 24. Results indicated that the ABR’s P4 latencies (neural transmission time) were significantly prolonged (worse) in the HAC pups and that ABR’s thresholds were significantly elevated (worse) in the HAC and MAC pups when compared to the CON pups. The HAC and MAC pups were also growth retarded and had higher postnatal mortality than the CON pups. The SAL and LAC pups showed little or no adverse effects. In conclusion, repeated AC treatment had harmful effects on the rat offspring’s ABRs, postnatal growth and survival. The prolonged ABR latencies reflect slowed neural transmission times along the auditory nerve and brainstem auditory pathway. The elevated ABR thresholds reflect hearing deficits. We concluded that repeated AC treatment can have harmful neurological, sensory and developmental effects on the rat offspring. These effects should be considered when weighing the benefits and risks of repeated AC treatment and when monitoring and managing the prenatally exposed child for possible adverse effects.

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Excess omega-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring

Cited by 46 publications

References 83 publications

Docosahexaenoic acid counteracts attenuation of CD95-induced cell death by inorganic mercury

Docosahexaenoic acid counteracts attenuation of CD95-induced cell death by inorganic mercury

Fish oil changes the lifespan of Caenorhabditis elegans via lipid peroxidation

Repeated antenatal corticosteroid treatments adversely affect neural transmission time and auditory thresholds in laboratory rats

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