## 3 Results and Discussion
### Antibiotic Susceptibility Testing Results  
The antibiotic sensitivity data presented in Tables 3 and 4 hold significant information regarding the influence of zinc salts on the antibiotic resistance of _E. coli_ and _E. faecalis_ strains. The results suggest that treating bacteria with zinc sulfate heptahydrate and zinc chloride alters bacterial sensitivity to various antibiotics, with notable differences observed for different bacterial species and antimicrobials. Our results indicate that zinc chloride tends to enhance susceptibility to a range of antibiotics in _E. coli_, particularly ciprofloxacin, amoxicillin, and mezlocillin. In contrast, susceptibility in _E. faecalis_ to cephalosporporins is reduced, suggesting a strain-specific action. The impact of zinc salts on antibiotic resistance has been investigated increasingly. [PERSON] et al. investigated zinc-resistant _E. coli_ isolates of environmental origin that were zntA-positive. They found that exposure to zinc increased resistance to ampicillin (92.6%) and amoxicillin(68.5%), but susceptibility to ciprofloxacin was not significantly affected [27]. This contrasts with our findings, in which zinc chloride enhanced susceptibility to ciprofloxacin in _E. coli_, showing strain-specific interaction with zinc. [PERSON] et al. demonstrated the role of zinc in altering antibiotic efficacy, with zinc enhancing bacterial sensitivity to \(\beta\)-lactam antibiotics, which corroborates our findings, where treatment with zinc chloride increased the zone of inhibition of amoxicillin in _E. faecalis_ ATCC 29212 [28]. On the other hand, _E. faecalis_ had decreased susceptibility to ceftaglime and ceftaxone, supporting the theory that exposure to zinc may enhance \(\beta\)-lactam resistance in some species. An increase in the ciprofloxacin zone of inhibition after treatment with  
\begin{table}
\begin{tabular}{c c c c c c c} \hline \hline \multirow{2}{*}{**ABG**} & \multicolumn{3}{c}{_E. coli_ **ATCC 14169**} & \multicolumn{3}{c}{_E. coli_ **ATCC 25922**} \\ \cline{2-7}  & **PC** & **ZnSO\({}_{\mathbf{4}}\times\mathbf{7H_{2}O}\)** & **ZnCl\({}_{\mathbf{2}}\)** & **PC** & **ZnSO\({}_{\mathbf{4}}\times\mathbf{7H_{2}O}\)** & **ZnCl\({}_{\mathbf{2}}\)** \\ \hline DXT 30 & 15.00 \(\pm\) 0.00 & 16.50 \(\pm\) 0.71 & 15.50 \(\pm\) 0.71 & 21.00 \(\pm\) 0.00 & 20.50 \(\pm\) 0.71 &  
zinc chloride suggests a possible synergistic effect, as previously observed. [PERSON] et al. reported that zinc-activated avobenzene possessed potent antibacterial activity against MRSA, highlighting the capacity of zinc to enhance fluoroquinolone activity [29]. Zinc exposure has also been reported to disrupt bacterial membrane integrity, which affects antibiotic uptake. This is also reflected in studies that suggest that zinc oxide nanoparticles can enhance the penetration of antibiotics, particularly aminoglycoses such as gentamicin [9]. This could explain the slight enhancement of gentamicin activity following zinc chloride treatment in our study. Exposure to zinc has been found to induce efflux pumps, leading to increased resistance to certain antibiotics [30]. Zinc exposure is linked to oxidative stress, which can either compromise bacterial defenses (sensitizing bacteria to antibiotics) or induce protective responses (increasing resistance). This was demonstrated by [PERSON] et al., who provided evidence that iron and zinc ions regulate efflux pumps and biofilm formation, thereby influencing multidrug resistance [31]. This work is founded on our earlier work on the effects of iron salts on microbial populations under such pipeline conditions [32]. There are interconnected trends in the two studies: large amounts of metals suppress biofilm development and microbial growth. At the same time, lower concentrations trigger stress-adaptive mechanisms in _E. coli_ and _E. faecalis_, including a change in antibiotic resistance. These findings suggest the need for carefully optimized dosing regimens to harness the antimicrobial action of metal ions without promoting resistance or the formation of biofilms.