Testicular cells

Tanphaichitr N, Sobhon P, Taluppeth N, Chalermisarachai P (1978) Basic nuclear proteins in testicular cells and ejaculated spermatozoa in man. Exp Cell Res 117 347-356... 

In the mid-pachytene stage of meiosis. Hit becomes preferentially enriched in testicular cells and contributes to up to 50% of the total chromosomal linker histones (Cole et al. 1986). The deletion of Hit has no effect on viability and fertility of mice (Drabent et al. 2000). It is not quite clear whether other HI variants are upregulated in pachytene spermatocytes of Hit-deficient animals and compensate for the loss of Hit (Drabent et al. 2003 Nayernia et al. 2005). Thus, very little is known about... 

Tanphaichitr, N., Sobhon, P., Taluppeth, N., and Chalermisarachai, P. (1978) Basic nuclear proteins in testicular cells and ejaculated spermatozoa in man. Exp. Cell Res. 117, 347-356. Palmer, D.K., O Day, K., and Margolis, R.L. (1990) The centromere specific histone CENP-A is selectively retained in discrete foci in mammalian sperm nuclei. Chromosoma 100, 32-36. 

Brown CD, Miller MG. 1989. Relationship between testicular cell culture age and susceptibility to 1,3-dinitrobenzene induced toxicity [Abstract], 28th Annual Meeting, Society of Toxicology, Atlanta, GA. 

Lloyd SC, Foster PMD. 1987. 1,3-Dinitrobenzene Toxicity and metabolism in rat testicular cell cultures. Arch Toxicol, SuppI 11 281-284. 

DBCP is a genotoxic in microbial and mammalian assays. The mechanism for DBCP-induced testicular toxicity may be related to direct DNA damage. Binding of DBCP metabolites to testicular cell DNA has been demonstrated. Alternatively, inhibition of sperm carbohydrate metabolism could also account for DBCP toxicity to epididymal sperm. 

Study on the effects of DNA damage induced by cigarette smoke in male mice testicular cells using comet assay. Wei Sheng Yan Jiu 2001 30(1) 28-30. 

The effects of diepoxybutane on male reproductive cells were investigated by flow cytometric and histological description of testicular cell populations and alterations of chromatin packaging. Male B6C3F mice were treated with a single intraperitoneal... 

The in-vitro metabolic activation of l,2-dibromo-3-chloropropane, measured as radio-label covalently bound to macromolecules, is three-fold faster in rat testicular cells than in human testicular cells (Bjorge et al., 1996a). 

The rate of metabolic activation of l,2-dibromo-3-chloropropane in httman testicular cells is abour one-third that of rat cells. No other data are available for comparison. Nevertheless, since P450 isoenzymes and several GST enzymes are rather similar in terms of substrate selectivity between httmans and rats, it is expected that httman tissues should be capable of activating l,2-dibromo-3-chloropropane via both P450- and GST-mediated pathways. 

DIA, DNA strand breaks, rat testicular cells in vitro + NT 1.2 Lag etal. (1989a)... 

In cultured mammalian cells, several studies have demonstrated the induction of DNA strand breaks (including one study w ith human primary testicular cell cultures), while (usually) single studies have demonstrated increases in the frequencies of gene mutations, sister chromatid exchanges, chromosomal aberrations and cell transformation. 

Bjorge, C., Wiger, R., Holme, J.A., Brunborg, G, Andersen, R., Dybing, E. Soderlund, E.J. (1995) In vitro toxicity of l,2-dibromo-3-chloropropane (DBCP) in different testicular cell types from rats. Reprod. Toxicol., 9, 461-473... 

DIA, DNA strand breaks, male Wistar rat liver and testicular cells + NT 3.5 Soderlund etal. (1992)... 

Smith, E.E., L.H. du Preez, B.A. Gentles, K.R. Solomon, B. Tandler, J.A. Carr, GJ. Van Der Kraak, RJ. Kendall, J.P. Giesy, and T.S. Gross (2005). Assessment of laryngeal muscle and testicular cell types in Xenopus laevis (Anura Pipidae) inhabiting maize and nonmaize growing areas of South Africa. AJ r. J. Herp., 54 69-76. 

The endogenous HMG-domain proteins in HeLa cell free extracts do not seem to affect the relative rates of repair of cisplatin-DNA adducts [54] [62], Nevertheless, the hypothesis that HMG-domain proteins can enhance cellular sensitivity to cisplatin by blocking repair of the DNA adducts is still viable. Several HMG-domain proteins are specifically expressed in the testes ([146] and references cited therein), two of which, tsHMG and hSRY, inhibit the in vitro excision of cisplatin-DNA adducts at lower protein concentrations than any of the other HMG-domain proteins tested [54] [146], Selective expression of these or other such proteins in testicular tumors would provide an explanation for the unusual cisplatin sensitivity of this tumor type and the reduced repair of cisplatin-DNA adducts observed in testicular cell lines (discussed above). 

Sister chromatid exchange analysis in spermatogonia Unscheduled DNA synthesis test (UDS) in testicular cells... 

Methoxyacetate inhibits lactate production by testicular cells in culture. 

Many compounds have been implicated as male reproductive toxicants, but their sites and mechanisms of action are not well understood. The classification of male reproductive toxicants as direct or indirect is useful to help define the primary site of toxicity (Figure 6). A direct toxicant would primarily target the testicular cells, the excurrent duct system of the male reproductive tract, or mature spermatozoa. An indirect toxicant would cause reproductive toxicity by acting on hypothalamic/pituitary neuroendocrine controls or on extragonadal systems. Since the testis is subject to hormonal control and feedback loops, the action of indirect toxicants on endocrine homeostasis can ultimately damage testicular cell types. 

In vitro systems have been developed to try and understand the mechanism of action of thiram alone and in the presence of other potentiating compounds. The genotoxic, cytotoxic, and neurotoxic effects of thiram have been studied using a variety of primary cultures as well as cell-lines. Lymphocytes exhibited sister chromatid exchanges and micronuclei with exposure to thiram. Thiram caused single-strand DNA breaks in testicular cells in vitro. Other studies indicate that thiram can be both clastogenic and mutagenic. 

DNP on energy-dependent cellular processes in testicular cells, rather than from a genotoxic effect. 

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