In the presence of an IAP of 15 mmHg, the bowel mucosa was less severely, but still significantly, damaged when compared to that of the controls (Table 6).
Further, the workers with CYP2D6*3 PM and PON1 (QQ and MM) genotypes were found to have significantly higher DNA damage when compared to other genotypes (p < 0.05).
Only the 2 mM dose of l-carnitine significantly (P < 0.01) decreased the rate of acrosomal damage when compared to the control group.
The catalytic activity of SOD is associated with the extent of lipid peroxidation as evidenced from the fact that SA treated plants results into the lower degree of membrane damage when compared to plants those were inoculated with the pathogen.
Mouse embryonic fibroblasts (MEFs) isolated from these transgenic mice showed an increased accumulation of DNA damage in cells exposed to oxidative damage when compared to MEFs from wild-type mice.
Guinea pigs immunized with BCG or rBCG85C showed a significant reduction in gross pathological damage, when compared to the saline treated animals.
However, animals immunized with rBCG85C showed a significantly reduced gross pathological damage, when compared to saline treated animals (p<0.05), as was evident from minimal involvement of the lungs with no evident sign of tissue damage in both liver and spleen (Fig. 2B).
Since, the haploid MATa variant of the hfi1Δ strain was described as hypersensitive to DOX, and both the ctk1Δ and hfi1Δ diploids display enhanced levels of mating with MATα tester strains (see below), we compared the relative sensitivity of the MATa haploid derivatives to DNA damage when compared to the WT counterpart.
Immunization with rBCG85C resulted in a substantial reduction in the lung (1.87 log10, p<0.01) and spleen (2.36 log10, p<0.001) bacillary load with a commensurate reduction in pathological damage, when compared to the animals immunized with the parent BCG strain at 10 weeks post-infection.
This showed ongoing areas of TIN with increased chronic damage when compared to the initial biopsy.
