Melatonin Ameliorates Developmental Landmarks Induced by Gestational and Lactational Coexposure to Chlorpyriphos and Cypermethrin in F1 Male Rats

The ameliorative potentials of melatonin (ML) on developmental changes evoked by gestational and lactational co-exposure to chlorpyriphos (CP) and cypermethrin (CY) was investigated in male Wistar rats. Pregnant dams were divided at random into 6 groups of 10 animals each and treated orally by gavage from gestation day 1 to postnatal day 21 with the following regimens: The DW, SO and ML groups were administered distilled water (2 ml/kg), soya oil (2 ml/kg) and melatonin (0.5 mg/kg), respectively; CC group was co-administered CP (1.9 mg/kg) and CY (7.5 mg/kg); MC group was pretreated with ML (0.5 mg/kg) and followed by co-administration of CP and CY while the CM group was administered CP and CY and then treated with ML. We evaluated the developmental parameters on the F1 generation male rats at different postnatal intervals following parturition. Alterations in litter size and weight, number of live/dead pups, anogenital distance, crown-rump length, time of eye and ear openings, and testicular descent induced by gestational and lactational exposure to CP and CY in F1 male rats were mitigated by pre- and post-administration of ML. These curative and prophylactic potentials of ML may be partly attributed to its widely known antioxidant property.

High-fat diet accelerate hepatic fatty acids synthesis in offspring male rats induced by perinatal exposure to nonylphenol

Background Low dose of NP exposure can alter adipose tissue formation, and the intake of high-fat diet (HFD) can also lead to the fatty liver disease. We investigated the combined effect of NP and HFD on the first offspring of rats, and whether this effect can be passed to the next generation and the possible mechanisms involved. Methods Pregnant rats had access to be treated with 5 μg/kg/day NP and normal diet. The first generation rats were given normal diet and HFD on postnatal day 21, respectively. Then the second generation rats started to only receive normal diet without NP or HFD. Body weight, organ coefficient of liver tissues, lipid profile, biochemical indexes and the expression of genes involved in lipid metabolism, as well as liver histopathology were investigated in male offspring of rats. Results NP and HFD interaction had significant effect on the birth weight, body weight and liver tissue organ coefficient of first generation male rats. And HFD aggravated abnormal lipid metabolism, even abnormal liver function and liver histopathological damage of first generation male rats produced by the NP. And this effect can be passed on to the second generation rats. HFD also accelerated the mRNA level of fatty acid synthesis genes such as Lpl, Fas, Srebp-1 and Ppar-γ of first generation rats induced by perinatal exposure to NP, even passed on to the second generation of male rats. NP and HFD resulted in synergistical decrease of the protein expression level of ERα in liver tissue in F2 male rats. Conclusion HFD and NP synergistically accelerated synthesis of fatty acids in liver of male offspring rats through reducing the expression of ERα, which induced abnormal lipid metabolism, abnormal liver function and hepatic steatosis. Moreover, all of these damage passed on to the next generation rats.

Paternal multigenerational exposure to an obesogenic diet drives epigenetic predisposition to metabolic diseases in mice

Obesity is a growing societal scourge. Recent studies have uncovered that paternal excessive weight induced by an unbalanced diet affects the metabolic health of offspring. These reports mainly employed single-generation male exposure. However, the consequences of multigenerational unbalanced diet feeding on the metabolic health of progeny remain largely unknown. Here, we show that maintaining paternal western diet feeding for five consecutive generations in mice induces an enhancement in fat mass and related metabolic diseases over generations. Strikingly, chow-diet-fed progenies from these multigenerational western-diet-fed males develop a 'healthy' overweight phenotype characterized by normal glucose metabolism and without fatty liver that persists for 4 subsequent generations. Mechanistically, sperm RNA microinjection experiments into zygotes suggest that sperm RNAs are sufficient for establishment but not for long-term maintenance of epigenetic inheritance of metabolic pathologies. Progressive and permanent metabolic deregulation induced by successive paternal western-diet-fed generations may contribute to the worldwide epidemic of metabolic diseases.

Ancestral plastics exposure induces transgenerational disease-specific sperm epigenome-wide association biomarkers

Plastic-derived compounds are one of the most frequent daily worldwide exposures. Previously a mixture of plastic-derived toxicants composed of bisphenol A, bis(2-ethylhexyl) phthalate, and dibutyl phthalate at low-dose exposures of a gestating female rats was found to promote the epigenetic transgenerational inheritance of disease to the offspring (F1 generation), grand-offspring (F2 generation), and great-grand-offspring (F3 generation). Epigenetic analysis of the male sperm was found to result in differential DNA methylation regions (DMRs) in the transgenerational F3 generation male sperm. The current study is distinct and was designed to use an epigenome-wide association study to identify potential sperm DNA methylation biomarkers for specific transgenerational diseases. Observations indicate disease-specific DMRs called epimutations in the transgenerational F3 generation great-grand-offspring of rats ancestrally exposed to plastics. The epigenetic DMR biomarkers were identified for testis disease, kidney disease, and multiple (≥2) diseases. These disease sperm epimutation biomarkers were found to be predominantly disease-specific. The genomic locations and features of these DMRs were identified. Interestingly, the disease-specific DMR-associated genes were previously shown to be linked with each of the specific diseases. Therefore, the germline has ancestrally derived epimutations that potentially transmit transgenerational disease susceptibilities. Epigenetic biomarkers for specific diseases could be used as diagnostics to facilitate clinical management of disease and preventative medicine.

Bisphenol A and 17α-ethinylestradiol-induced transgenerational gene expression differences in the brain–pituitary–testis axis of medaka, Oryzias latipes†

Endocrine disrupting chemicals (EDCs), such as bisphenol A (BPA) and 17α-ethinylestradiol (EE2), can have far reaching health effects, including transgenerational abnormalities in offspring that never directly contacted either chemical. We previously reported reduced fertilization rates and embryo survival at F2 and F3 generations caused by 7-day embryonic exposure (F0) to 100 μg/L BPA or 0.05 μg/L EE2 in medaka. Crossbreeding of fish in F2 generation indicated subfertility in males. To further understand the mechanisms underlying BPA or EE2-induced adult onset and transgenerational reproductive defects in males, the present study examined the expression of genes regulating the brain–pituitary–testis (BPT) axis in the same F0 and F2 generation male medaka. Embryonic exposure to BPA or EE2 led to hyperactivation of brain and pituitary genes, which are actively involved in reproduction in adulthood of the F0 generation male fish, and some of these F0 effects continued to the F2 generation (transgenerational effects). Particularly, the F2 generation inherited the hyperactivated state of expression for kisspeptin (kiss1 and kiss2) and their receptors (kiss1r and kiss2r), and gnrh and gnrh receptors. At F2 generation, expression of DNA methyltransferase 1 (dnmt1) decreased in brain of the BPA treatment lineage, while EE2 treatment lineage showed increased dnmt3bb expression. Global hypomethylation pattern was observed in the testis of both F0 and F2 generation fish. Taken together, these results demonstrated that BPA or EE2-induced transgenerational reproductive impairment in the F2 generation was associated with alterations of reproductive gene expression in brain and testis and global DNA methylation in testis.

Paternal multigenerational exposure to an obesogenic diet drives epigenetic predisposition to metabolic disorders

Obesity is a growing societal scourge responsible for approximately 4 million deaths worldwide. Recent studies have uncovered that paternal excessive weight induced by an unbalanced diet affects the metabolic health of offspring. These reports mainly employed single-generation male exposure. However, the consequences of multigenerational unbalanced diet feeding on the metabolic health of progeny remain largely unknown. Here, we show that maintaining paternal western diet feeding for five consecutive generations in mice induces a gradual enhancement in fat mass and related metabolic diseases over generations. Strikingly, chow-diet-fed progenies from these multigenerational western-diet-fed males develop a “healthy” overweight phenotype that is not reversed after 4 subsequent generations. Mechanistically, sperm RNA microinjection experiments into zygotes suggest that sperm RNAs are sufficient for establishment but not for long-term maintenance of epigenetic inheritance of metabolic pathologies. Progressive and permanent metabolic deregulation induced by successive paternal western-diet-fed generations may contribute to the worldwide epidemic of metabolic diseases.

Steinernema bertusi n. sp. (Rhabditida: Steinernematidae), a new entomopathogenic nematode from South Africa

Summary Two isolates of Steinernema bertusi n. sp. were separately recovered from Tito, Mpumalanga, and Port Edward, Kwa Zulu Natal, South Africa. In this paper, we describe the isolates as a new entomopathogenic nematode (EPN) species using molecular and morphological methodologies. The new species belongs to the cameroonense-clade, which consists of nematodes only isolated from the African continent. Steinernema bertusi n. sp. is characterised by having the longest infective juvenile (IJ) for this clade at 716 (628-814) μm. The IJ is further characterised by a body diam. of 32 (28-36) μm and the pattern for the arrangement of the lateral ridges from head to tail is 2, 4, 5, 4, 2. The first-generation male spicule and gubernaculum length is 82 (72-88) μm and 63 (54-72) μm, respectively. Only 25% of the second-generation males possess a mucron. The first-generation females of S. bertusi n. sp. have a slightly protruding vulva, with double-flapped epiptygmata and a mucron at the posterior end. The new EPN species is most closely related to S. sacchari and is the sixth species to be included in the cameroonense-clade.

Mizrahim masculine fashion as the expression of political confrontation in Israel in the 1970s

This article explores how and why, in the 1970s, Israeli Mizrahi men – Jews from Arab countries – used fashion (among other tools) to both rebel against Ashkenazim hegemony and reconnect with their own roots. This article first shows how, during Israel’s pre-state era, many Jewish Ashkenazim pioneers wore a very simple outfit that was associated with socialist political ideology and became the male Israeli national dress code before and after Israel’s establishment in 1948. Not all Israelis identified with it, though: in the 1970s, second-generation male Mizrahim rebelled against the ethnic and racial discrimination they suffered from Ashkenazim, and used fashion alongside other means to express their opposition. By doing so, Mizrahim paved the way for contemporary male Israeli fashion. This article clarifies how this fashion change occurred, and how it converged with political upheaval. It also discloses the links with Mizrahim Arabic heritage concerning body care.