Further observations on carbendazim-induced abnormalities of spermatid morphology in rats

Nakai, Michikazu; Hess, Rex A.; Matsuo, Fusako; Gotoh, Yukitoshi; Nasu, Tetsuo

doi:10.1016/s0040-8166(97)80033-x

Cited by 16 publications

(6 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, nucleation and stabilization of manchette microtubules in a directed manner on the spermatid nucleus could be accomplished through a common signaling mechanism. Acrosome formation is dependent on microtubules and shares features with vesicle transport in other systems [37,38]. The KRP3B staining in early spermatids before formation of the acrosome is very similar to the placement and structure of the Golgi apparatus in these cells.…”

Section: Discussionmentioning

confidence: 66%

KRP3A and KRP3B: Candidate Motors in Spermatid Maturation in the Seminiferous Epithelium1

Zou¹,

Millette²,

Sperry³

2002

Biology of Reproduction

View full text Add to dashboard Cite

We have identified KRP3, a novel kinesin-related protein expressed in the mammalian testis, and have examined the tissue distribution and subcellular localization of isoforms of this protein. Isolation of KRP3 clones, using the head domain identified in a previous PCR screen as probe, identified at least two KRP3 isoforms in the rat. We have isolated coding sequences of two highly related cDNAs from the rat testis that we have termed KRP3A and KRP3B (kinesin-related protein 3, A and B). Both cDNAs code for predicted polypeptides with the three-domain structure typical of kinesin superfamily members; namely a conserved motor domain, a region capable of forming a limited coiled-coil secondary structure, and a globular tail domain. Although almost identical in their head and stalk domains, these motors diverge in their tail domains. This group of motors is found in many tissues and cell types. The KRP3B motor contains DNA-binding motifs and an RCC1 (regulator of chromosome condensation 1) consensus sequence in its tail domain. Despite this similarity, KRP3B is not associated with the same structures as RCC1. Instead, KRP3 isoforms localize with the nuclei of developing spermatids, and their immunolocalization in the testis overlaps with that of the small GTPase Ran. Like Ran, KRP3 motors are associated in a polarized fashion with the nucleus of maturing spermatids at various stages of elongation. Our findings suggest a possible role for KRP3 motor isoforms in spermatid maturation mediated by possible interaction with the Ran GTPase.

show abstract

Section: Discussionmentioning

confidence: 66%

KRP3A and KRP3B: Candidate Motors in Spermatid Maturation in the Seminiferous Epithelium1

Zou¹,

Millette²,

Sperry³

2002

Biology of Reproduction

View full text Add to dashboard Cite

show abstract

“…For CBZ, no changes were observed in Inhibin B at either dose level (100 and 400 mg/kg/day) even though there were grade 1 to 2 findings at the low dose and grades 2 and 4 at the high dose. This lack of correlation may be a function of the mechanism of CBZ with disruption of Sertoli cell microtubules causing abnormal spermatocytes and spermatids with giant and multinucleate spermatids (Nakai et al., , and Nakai and Hess, ) without direct Sertoli cell toxicity. With a single dose of EDS there was grade 4 Leydig cell degeneration on SD 1 with no change in Inhibin B.…”

Section: Discussionmentioning

confidence: 99%

“…Nitrofurazone is a seminiferous tubule germ cell toxicant that causes single strand DNA breakage and damage loss of round spermatocytes and elongate spermatids (Olive and McCalla, ; Nishimura et al., ; Shoda et al., ; Hagenas et al., ), 2,5‐hexanedione (2,5‐HD) is a neurotoxicant that also disrupts spermiation with findings including Sertoli cell vacuolation, spermatid retention, and complete depletion of germ cells (Boekelheide, ; Fleming et al., ; Moffit et al., ). The fungicide carbendazim (CBZ) disrupts Sertoli cell microtubules resulting in abnormal spermatocytes and spermatids with giant and multinucleate spermatids (Carter et al., ; Nakai et al., , ; Nakai and Hess, ). DL‐ethionine, is a methionine analog and germ cell toxicant that disrupts protein synthesis resulting in degeneration, necrosis, and loss of all germ cell stages (Kaufman et al., ).…”

Section: Introductionmentioning

confidence: 99%

Inhibin B Response to Testicular Toxicants Hexachlorophene, Ethane Dimethane Sulfonate, Di‐(n‐butyl)‐phthalate, Nitrofurazone, DL‐Ethionine, 17‐alpha Ethinylestradiol, 2,5‐Hexanedione, or Carbendazim Following Short‐Term Dosing in Male Rats

Erdős

Pearson

Goedken

et al. 2013

Birth Defects Research Pt B

View full text Add to dashboard Cite

show abstract

“…Many agents have been shown to induce manchette abnormalities, including inhibitors of microtubule dynamics (such as carbendezim and taxol) and of RNA/DNA synthesis as well as alkylating agents. 30,36 Manchette dysfunction is also seen in a variety of genetically modified mouse models, reviewed in. 3,27,30 Ectopic manchettes are commonly observed (e.g., 25,30,31,37 ) and the position and direction of the microtubules then determine the type of deviations on nuclear surface.…”

Section: Abnormal Sperm Head Shapementioning

confidence: 99%

Mechanisms of spermiogenesis and spermiation and how they are disturbed

2014

View full text Add to dashboard Cite

Haploid round spermatids undergo a remarkable transformation during spermiogenesis. The nucleus polarizes to one side of the cell as the nucleus condenses and elongates, and the microtubule-based manchette sculpts the nucleus into its species-specific head shape. The assembly of the central component of the sperm flagellum, known as the axoneme, begins early in spermiogenesis, and is followed by the assembly of secondary structures needed for normal flagella. The final remodelling of the mature elongated spermatid occurs during spermiation, when the spermatids line up along the luminal edge, shed their residual cytoplasm and are ultimately released into the lumen. Defects in spermiogenesis and spermiation are manifested as low sperm number, abnormal sperm morphology and poor motility and are commonly observed during reproductive toxicant administration, as well as in genetically modified mouse models of male infertility. This chapter summarizes the major physiological processes and the most commonly observed defects in spermiogenesis and spermiation, to aid in the diagnosis of the potential mechanisms that could be perturbed by experimental manipulation such as reproductive toxicant administration. Signature LesionThere are a number of signature lesions that could indicate a disturbance in spermiogenesis or spermiation. These would include misshapen heads and/or tails of elongating/elongated spermatids. Multinucleated round spermatids may reflect disturbances in spermiogenesis, but could also reflect altered Sertoli cell function. Disruption of spermiation could present itself as spermatid retention at the lumen of post stage VIII tubules, failure of elongated spermatids to ascend to the lumen of stage VII/ VIII tubules, or phagocytosis of mature spermatids at the base of tubules in stages VII through to approximately XII (in mice) or XIV (in rats). The changes might occur in isolation or in combination with one another.

show abstract

Further observations on carbendazim-induced abnormalities of spermatid morphology in rats

Cited by 16 publications

References 30 publications

KRP3A and KRP3B: Candidate Motors in Spermatid Maturation in the Seminiferous Epithelium1

KRP3A and KRP3B: Candidate Motors in Spermatid Maturation in the Seminiferous Epithelium1

Inhibin B Response to Testicular Toxicants Hexachlorophene, Ethane Dimethane Sulfonate, Di‐(n‐butyl)‐phthalate, Nitrofurazone, DL‐Ethionine, 17‐alpha Ethinylestradiol, 2,5‐Hexanedione, or Carbendazim Following Short‐Term Dosing in Male Rats

Mechanisms of spermiogenesis and spermiation and how they are disturbed

Contact Info

Product

Resources

About