Aqueous Extract of Adansonia digitata reversed Cotton Seed Extract-Induced Testicular Damage in Wistar rats.

OBJECTIVE: Infertility is the inability of sexually active couples without using birth control to get pregnant after one year of uninterrupted sexual intercourse. Cotton Seed Extract (CSE) has been linked to male infertility by causing oxidative damage to the testes due to the action of its active component, Gossypol. Adansonia digitata has been known to have many medically useful properties, including antioxidant effects. This study aimed at evaluating the effects of Adansonia digitata on Cottonseed extract-induced testicular damage. METHODS: Forty (40) Adult male Wistar rats were divided into 8 groups of five rats per group (n=5). Group 1 served as the control and received 0.5 ml of phosphate buffer orally; Group 2 received 800 mg/kg b.wt A. digitata orally; Group 3 received 300 mg/kg b.wt Vitamin E only orally; Group 4 received 60 mg/kg b.wt CSE intraperitoneally; Group 5 received 20 mg/kg b.wt CSE intraperitoneally; Group 6 received 60 mg/kg b.wt CSE intraperitoneally and 800 mg/kg b.wt A. digitata orally; Group 7 received 20 mg/kg b.wt CSE intraperitoneally and 800 mg/kg b.wt A. digitata orally; Group 8 received 60 mg/kg b.wt CSE intraperitoneally and 300 mg/kg Vit. E orally. It was administered for 21 days. The testes and epididymis were dissected following abdominal incision. The epididymis was used for semen analysis while the testes was processed for histological analysis and biochemical assay. All the data was analyzed by ANOVA, using the SPSS version 17.0 software. A p<0.05 was considered significant. RESULTS: CSE administration caused significant (p<0.05) decrease in sperm count, found in the group treated with CSE only. However, the Administration of A. digitata caused significant increase (p<0.05) in sperm count, G6PDH, LDH, GPx and SOD; however, MDA levels were decreased. Histological observations showed a decrease in the number of Spermatogonia and differentiating cells in the testes of rats treated with CSE. CONCLUSIONS: The results obtained revealed the antioxidant ability of A. digitata in counter-acting the testicular damage caused by CSE administration.

Biochemical changes on the repair of surgical bone defects grafted with biphasic synthetic micro-granular HA + ß-tricalcium phosphate induced by laser and LED phototherapies and assessed by Raman spectroscopy.

This work aimed the assessment of biochemical changes induced by laser or LED irradiation during mineralization of a bone defect in an animal model using a spectral model based on Raman spectroscopy. Six groups were studied: clot, laser (λ = 780 nm; 70 mW), LED (λ = 850 ± 10 nm; 150 mW), biomaterial (biphasic synthetic micro-granular hydroxyapatite (HA) + ß-tricalcium phosphate), biomaterial + laser, and biomaterial + LED. When indicated, defects were further irradiated at a 48-h interval during 2 weeks (20 J/cm2 per session). At the 15th and 30th days, femurs were dissected and spectra of the defects were collected. Raman spectra were submitted to a model to estimate the relative amount of collagen, phosphate HA, and carbonate HA by using the spectra of pure collagen and biomaterials composed of phosphate and carbonate HA, respectively. The use of the biomaterial associated to phototherapy did not change the collagen formation at both 15 and 30 days. The amount of carbonate HA was not different in all groups at the 15th day. However, at the 30th day, there was a significant difference (ANOVA, p = 0.01), with lower carbonate HA for the group biomaterial + LED compared to biomaterial (p < 0.05). The phosphate HA was higher in the groups that received biomaterial grafts at the 15th day compared to clot (significant for the biomaterial; p < 0.01). At the 30th day, the phosphate HA was higher for the group biomaterial + laser, while this was lower for all the other groups. These results indicated that the use of laser phototherapy improved the repair of bone defects grafted with the biomaterial by increasing the deposition of phosphate HA.

Independent origins of loss-of-function mutations conferring oxamniquine resistance in a Brazilian schistosome population.

Molecular surveillance provides a powerful approach to monitoring the resistance status of parasite populations in the field and for understanding resistance evolution. Oxamniquine was used to treat Brazilian schistosomiasis patients (mid-1970s to mid-2000s) and several cases of parasite infections resistant to treatment were recorded. The gene underlying resistance (SmSULT-OR) encodes a sulfotransferase required for intracellular drug activation. Resistance has a recessive basis and occurs when both SmSULT-OR alleles encode for defective proteins. Here we examine SmSULT-OR sequence variation in a natural schistosome population in Brazil ∼40years after the first use of this drug. We sequenced SmSULT-OR from 189 individual miracidia (1-11 per patient) recovered from 49 patients, and tested proteins expressed from putative resistance alleles for their ability to activate oxamniquine. We found nine mutations (four non-synonymous single nucleotide polymorphisms, three non-coding single nucleotide polymorphisms and two indels). Both mutations (p.E142del and p.C35R) identified previously were recovered in this field population. We also found two additional mutations (a splice site variant and 1bp coding insertion) predicted to encode non-functional truncated proteins. Two additional substitutions (p.G206V, p.N215Y) tested had no impact on oxamniquine activation. Three results are of particular interest: (i) we recovered the p.E142del mutation from the field: this same deletion is responsible for resistance in an oxamniquine selected laboratory parasite population; (ii) frequencies of resistance alleles are extremely low (0.27-0.8%), perhaps due to fitness costs associated with carriage of these alleles; (iii) that four independent resistant alleles were found is consistent with the idea that multiple mutations can generate loss-of-function alleles.