Disease relevance of Ldhc

• Highly significant correlation between parameters of infertility like reduced cauda sperm count, and implantation sites, and reduction in LDH-X activity of cauda epididymal sperm and carnitine levels in cauda epididymal fluid were observed [1].

High impact information on Ldhc

• This report describes developments toward a cell specific-locus test for measuring point mutations directly in sperm based upon the use of a monospecific antibody against sperm-specific lactate dehydrogenase-X (LDH-X) [2].
• The amino acid sequence of 85% of the 330 residues from rat LDH-C subunit has been unambiguously determined, and the sequences of the remaining regions were tentatively aligned on the basis of peptide compositions and sequence homologies with the other known lactate dehydrogenase sequences, including mouse LDH-C [3].
• In contrast, germ cell (lactate dehydrogenase-C, phosphoglycerate kinase-2, and protamine-1) mRNA levels increased to the greatest extent between 1-4 weeks after the start of testosterone treatment and, after a short lag period, reflected increases in germ cell type and number [4].
• In the rat lactate dehydrogenase C exists in two molecular forms, isoenzymes C4 and A1C3 [5].
• Lactate dehydrogenase C, an isoenzyme composed of C polypeptide subunits and found only in mature testes and spermatozoa, differs kinetically, chemically and immunologically from the five common isoenzymes of lactate dehydrogenase, each of which is a tetramer of A and/or B subunits [5].

Biological context of Ldhc

• The results were similar with regard to testicular LDH-X activity and histology [6].
• At 5 weeks after the cessation of gossypol treatment, the spermatozoal LDH-X activity had only partially recovered but the fertility (number of ejaculated sperm, embryo implantation sites and pups born) had recovered to a level comparable to the control values 5 weeks after the cessation of gossypol treatment [7].
• Dose effect relations of inhaled EO on spermatogenesis were evaluated from testicular and epididymal weights, histopathological changes and lactate dehydrogenase X (LDH X) activity in the testis, and sperm counts and sperm head abnormalities in the epididymis [8].
• Total LDH and LDH X activities in testis exhibited circadian rhythms with different timing [9].
• LDH-X activity and serum testosterone levels were similar for both genotypes at 180 days of age [10].

Anatomical context of Ldhc

• Testicular LDH-X activity, a pachytene spermatocyte marker enzyme, was significantly decreased in animals by the eighteenth day of treatment with diglyme [11].
• In the present study, the effects of racemic gossypol and the (+) and (-) optical isomers of gossypol on LDH-X derived from rat and hamster testicular cytosol are compared to determine if there is any correlation between the in vitro inhibition of the LDH-X enzyme and in vivo antifertility effects [12].
• It was found to inhibit rat testis cytosolic LDH-X activity, in vitro, in a dose-dependent manner [13].
• Groups of control and gossypol-treated rats were sacrificed at 2-, 4-, and 5-week intervals when LDH-X analysis of spermatozoa were prepared from the tail of the epididymis [7].
• Decrease in testicular weight due to EtO exposure was completely prevented by methylcobalamin, and decrease in testicular mature spermatid count and LDH-X activity was fairly well prevented [14].

Associations of Ldhc with chemical compounds

• Inhibition of LDH-X by gossypol optical isomers [12].
• Despite a small reduction in testicular and epididymal glutathione levels 12 h after exposure to 2000 mg/kg acetochlor, testicular LDH and LDH-X enzyme levels were unaffected [15].
• CONCLUSIONS: These findings suggest that CdCl2 induces impairment of testicular function and causes a marked reduction in testicular LDH-X activity; that LDH-X activity is a biological marker of testicular damage; and that, except at high doses of CdCl2, this damage can be prevented by oxypurinol or SOD [6].
• Dose and time related changes in LDH-X activity, epididymal carnitine levels and fertility, in gossypol-treated male rats [1].
• Results revealed that ofloxacin, ciprofloxacin and pefloxacin reduced testicular LDH-X activity by 39.8%, 62.7% and 60.7%, respectively [16].

Other interactions of Ldhc

• LDH B remained fairly constant, and LDH C increased from undetectable levels at birth to become the most abundant of the three polypeptides from week 3 onwards [17].
• Among the marker enzymes of the testicular cells, LDH-X activity decreased, and beta-glucuronidase activity, cytochrome P-450 content and cytochrome b5 content increased in the 1000 mg/kg group [18].

Analytical, diagnostic and therapeutic context of Ldhc

• Lactate dehydrogenase-C, phosphoglycerate kinase-2, protamine-1, and sulfated glycoprotein-2 mRNA levels (on a per micrograms RNA basis) were 34%, 34%, less than 1%, and 580% of control values, respectively, 4 weeks after hypophysectomy and 79%, 87%, 61%, and 192% of control values, respectively, after 8 weeks of testosterone treatment [4].
• No differences in testis weight, morphology, or LDH-X enzyme activity were found between allograft and isograft recipients [19].

References